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Diseases » Grand mal seizures » Diagnosis
 

Diagnosis of Grand mal seizures

Grand mal seizures Diagnosis: Book Excerpts

Diagnosis of Grand mal seizures: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Grand mal seizures:

Diagnostic Tests for Grand mal seizures: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Grand mal seizures.


FACIAL PARALYSIS: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it acute or gradual onset? If it is acute onset, Bell's palsy, diabetic neuropathy, and cerebral vascular accident must be considered. If it is gradual onset, one must consider an acoustic neuroma, advancing petrositis, or a brain tumor or abscess.
  2. Is there associated hemiplegia or hemiparesis? If there is associated hemiplegia or hemiparesis and it is acute onset, one should consider cerebral vascular accident or extradural or subdural hematoma. If the hemiparesis, however, is contralateral, one should consider a brain stem thrombosis or hemorrhage. There are two clinical syndromes that are due to basilar artery lesions: Foville's syndrome and Millard-Gubler syndrome. If the hemiparesis is gradual onset, one should consider brain tumor or abscess or degenerative disease.
  3. Is there earache or hearing loss? Associated earache or hearing loss should make one think of acoustic neuroma, petrositis, mastoiditis, herpes zoster, and cholesteatoma.

DIAGNOSTIC WORKUP

Immediate referral to a neurologist is indicated. One should do a complete examination of the ear, nose, and throat to determine if there is any rupture of the drum, discharge, evidence of otitis media, etc. Then x-rays of the mastoids and petrous bones should be done along with tomography. A CT scan of the brain with emphasis on the internal auditory foramina should be done if acoustic neuroma is suspected. Culture of the discharge from the ears and blood culture should be done if there are associated signs of an infectious process. Testing for Lyme disease may be indicated. Spinal fluid analysis should be done to look for Guillain-Barré syndrome. If myasthenia gravis is suspected, a Tensilon test may be done. Spinal fluid culture should be done in cases of brain abscess. Carotid scans and a workup for an embolic source should be done in cases of cerebral vascular accident. Of course, when there is a brain tumor or abscess or a cerebral vascular accident is suspected, CT scans of the brain should be done. If these are not helpful or are inconclusive, MRI of the brain can be done. Glucose tolerance testing should be done to rule out diabetic neuropathy. If lead poisoning is suspected, a blood level for lead should be done.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Aura: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Epilepsy
    –Recurrent seizures
    –Strong family history
  • Migraine with aura
    –Usually visual aura (e.g., scotoma, flashing lights) lasting less than 60 minutes
    –Usually fully reversible with rare migrainous infarction (like CVA)
    –Migraine headache follows aura within 60 minutes and lasts 4–72 hours; however, aura may occur without headache
    • Partial seizure
      –60% of patients with focal seizures have an accompanying aura
      –Aura symptoms are associated with the brain area where they originate (e.g., occipital lobe seizure results in seeing lights)
      –Simple partial seizures result in focal tonic-clonic motor activity without loss of consciousness
      –Complex partial seizures progress to decreased consciousness and unresponsiveness
    • Tonic-clonic (grand mal seizure) seizures result in an abrupt loss of consciousness followed by stiffness (tonic); the patient then starts jerking (clonic) for an additional 2–3 minutes; rare aura
    • Pituitary adenoma or other underlying pathology that predisposes to migraines, seizures, or altered sensations (taste, smell)
    • Hallucinations (not actually an aura)
      • Physiologic nonepileptic seizures
        –Usually due to an underlying physiologic cause (e.g., fever, hypoglycemia, hypo- or hyperthyroidism, renal failure, cerebral anoxia)
    • Absence seizures (petit mal seizure) only rarely have an aura

    Workup and Diagnosis

    • History is very important
      –Type of aura (any of five senses)
      –Loss of consciousness
      –Associated activities and triggers (e.g., stress, medications, exertion, trauma, foods)
      –Postaura symptoms (e.g., headache, loss of consciousness, seizure)
      –History or family history of seizures or migraines
      –Review past medical history for head injury, stroke, dementia, intracranial infection, and alcohol or drug abuse
      –Full head, neck, and neurologic exam (look for one-sided features that suggest pathology on opposite side of brain)
      –Examine for trauma following loss of consciousness
    • Initial tests may include glucose, electrolytes, calcium, magnesium, CBC, BUN/creatinine, and toxicology screen
      • EEG may be indicated if seizure activity is suspected
        (provocative EEG with triggers gives higher yield)
        –Normal EEG does not rule out epilepsy
        –May be abnormal in migraines
      • MRI to rule out cerebral pathology
      • CT if physiologic seizure or trauma is involved (not indicated in patients with migraine and normal neurologic exam unless pattern of migraine has changed)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Chorea: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Huntington's disease (chronic progressive hereditary chorea)
    –Autosomal dominant transmission
    –Associated with psychiatric symptoms and progressive dementia
    –Caudate atrophy on neuroimaging studies
    –Marker on chromosome 4
    • Sydenham's chorea
      –Symptoms follow febrile illness (20–30%
      of cases are associated with group A strep)
      –Seen in rheumatic fever
      –Peak ages: 5–13 years
      –More common in females
  • Systemic lupus erythematosus
  • AIDS
  • Hyperthyroidism
    • Chorea gravidarum
      –Develops in the first 4–5 months of
      pregnancy
      –Resolves following delivery
  • Drug-induced (e.g., levodopa, stimulants, anticonvulsants, antidepressants, neuroleptics, oral contraceptives)
  • Stroke
  • Neoplasm
    • Wilson's disease
      –Autosomal recessive disorder
      –Deficiency in copper metabolism
      –Associated with hepatic dysfunction,
      dystonia, dysarthria
  • Benign hereditary chorea
    –Autosomal dominant
    –Onset before age 5
    –Symptoms are nonprogressive
    • Neuroacanthocytosis
      –Etiology unknown
      –Characterized by chorea and deformed
      erythrocytes
  • DRPLA
    –Most common in Japan
    –Characterized by chorea, ataxia, epilepsy, and dementia

    • Workup and Diagnosis

    • History and physical examination
      –Clinical diagnosis is sufficient for Sydenham's chorea
      –Huntington's disease may present with psychiatric symptoms (e.g., depression) before other manifestations; onset of symptoms typically occurs in the fourth and fifth decades of life
      –The appearance of Kayser-Fleischer rings in the cornea on slit-lamp exam is diagnostic for Wilson's disease
    • Neuroimaging (CT, MRI) to rule out mass lesions and Huntington's disease (cerebral/basal ganglion atrophy)
    • Genetic testing for Huntington's disease
    • Echocardiography to diagnose carditis
    • Throat culture or serology (ASO) for streptococcal infection
    • Low level of serum ceruloplasmin and elevated 24-hour urine copper in Wilson's disease
    • Thyroid function tests to rule out hyperthyroidism
    • ANA to rule out lupus
    • Neuroacanthocytosis: Acanthocytes appear on peripheral smear with clinical symptoms of chorea, dystonia, and tics
    • DRPLA: Imaging studies may reveal cerebral and cerebellar atrophy

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Seizures/Convulsions: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    • Partial seizure (involve only part of the brain)
      –Simple (no altered consciousness)
      –Complex (with altered consciousness)
    • Generalized seizure (involve both hemispheres)
      –Tonic-clonic
      –Atonic
      –Tonic
      –Myoclonic
      –Absence
    • Epilepsy
      –Recurrent unprovoked seizures of any or multiple types, which may be idiopathic or symptomatic
      • Secondary seizure
        –Metabolic abnormalities (e.g., electrolyte disturbances, hypoglycemia)
        –Drug effects, intoxication, or withdrawal
        –Head injury/trauma
        –Febrile seizures in children
        –Structural lesions (e.g., tumor, subdural hematoma)
        –Cerebrovascular etiologies (e.g., cerebral infarct, intracerebral hemorrhage, subarachnoid hemorrhage
        –Hypoxic-ischemic encephalopathy
        –Infection (e.g., meningitis, encephalitis)
        –Hypoxia
      • Nonepileptic seizure
        –Not associated with abnormal electrical activity in the brain
        –Patients with loss of consciousness secondary to cerebral hypoperfusion (fainting, syncope) may occasionally exhibit brief periods of twitching or convulsive movements resembling seizure activity
        –Psychological disturbances (pseudoseizure)
      • Inborn errors of metabolism
        –Disorders of amino acid metabolism
        –Organic acidemias
        –Urea cycle disorders
        –Mitochondrial disorders
        –Peroxisomal disorders
        –Glycogen storage disorders
        –Disorders of sugar metabolism
      • Rasmussen's encephalitis
        –Causes seizures and progressive hemispheric dysfunction in infants

      Workup and Diagnosis

      • History and physical examination
        –In many instances, the most useful history is obtained from a witness of the seizure rather than the patient him- or herself, because seizures commonly cause altered consciousness and may result in postictal confusion
        –Appropriate classification of seizure type may help to suggest etiology and treatment (e.g., a partial seizure resulting in isolated clonic jerking of the right arm is suggestive of pathology in the left frontal lobe)
        –Evidence of postictal paralysis on examination may also help to suggest the part of the brain involved
      • Initial labs should include CBC, electrolytes, glucose, O2 saturation, calcium, magnesium, glucose, and BUN/creatinine
      • CT is suitable for emergent evaluation, but MRI is more sensitive
      • CSF examination if CNS infection (e.g., meningitis) or subarachnoid hemorrhage is suspected
      • Drug screen and ethanol level
      • EEG
      • Video EEG monitoring may be useful in cases of refractory epilepsy as part of evaluation for epilepsy surgery or suspected nonepileptic seizures

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Facial Paralysis & Bell's Palsy: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    • Bell's palsy (idiopathic facial palsy of lower motor neuron type)
      –Most common cause of facial nerve paralysis
  • Lyme disease
  • Tumors that invade the temporal bone (e.g., cholesteatoma, carotid body tumor)
  • Ramsay Hunt's syndrome
    –Association of facial palsy with herpes zoster eruption in the pharynx and external auditory canal
    –Eighth cranial nerve often affected as well
    • Acoustic neuroma
      –May compress the facial nerve
    • Pontine lesions
      –Secondary to infarcts, demyelinating processes, or tumors
      –Signs of brainstem involvement may be associated
    • Facial diplegia or bilateral facial palsy
      –Guillain-Barré syndrome (associated with ascending areflexic motor paralysis)
      –Heerfordt's syndrome (a form of sarcoidosis; also known as uveoparotid fever)
  • Diabetic neuropathy
  • Leprosy
    • Melkersson-Rosenthal syndrome
      –Recurrent facial palsy, labial edema, and tongue plication
  • Sarcoidosis

    • Workup and Diagnosis

    • History and physical examination, with complete ENT and neurologic exams
      –Associated neurologic deficits may occur (e.g., weakness of the arm or leg, aphasia) due to involvement of surrounding brain areas in a vascular event
      –Depending on the site of interruption, the patient may have hyperacusis, a loss of taste over the anterior 2/3 of tongue, deafness, tinnitus, dizziness, or associated brainstem signs
      –Bell's palsy is a clinical diagnosis with testing reserved for atypical presentations or slowly resolving cases; make sure there are no herpetic lesions in the pharynx or external auditory canal; also pay special attention to assessing the eighth cranial nerve, as it courses very close to the facial nerve
    • Initial labs may include CBC, glucose, ESR, and Lyme titer
    • Head MRI
    • In cases of supranuclear palsy, a workup for CVA, demyelinating processes, and/or tumors may be indicated; include CT, MRI, and CSF studies

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Chorea: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

      • Toxins
        –Neuroleptics, phenytoin, antiemetics, oral contraceptives, theophylline, L-dopa, stimulants, lithium, carbon monoxide, manganese
    • Sydenham chorea (in rheumatic fever)
      –Migratory chorea, hypotonia, dysarthria, emotional liability
      –Usually 4 months after group A β-hemolytic Streptococcus infection
      –Molecular mimicry between streptococcal and CNS antigens results in formation of cross-reactive antibodies that disrupt basal ganglia function
      –Carditis is present in 80% of Sydenham chorea patients
        • Inherited choreas
          –Benign familial chorea
          –Juvenile Huntington chorea (usually presents with rigidity)
          –Familial paroxysmal choreoathetosis
      • Postinfectious: Mycoplasma, HSV, EBV, echovirus 25, varicella
      • Encephalitis: viral, mycoplasma, Lyme
      • Post-cardiac surgery
        –“Post-pump chorea”
        –Usually 2 weeks after cardiac surgery
      • Syndrome or disease associated
        –Wilson disease
        –Hallervorden-Spatz (disorder of iron metabolism with degeneration of globus pallidus)
        –Fahr disease: Encephalopathy and progressive calcification of basal ganglia
        –Lesch-Nyhan syndrome
        –Ataxia-telangiectasia
      • Endocrine: Hyperthyroidism, pregnancy (chorea gravidarum)
        • Acquired brain disorders
          –Multiple sclerosis, basal ganglia stroke, hypoxic ischemic encephalopathy, neoplasm
      • Abetalipoproteinemia
      • Glutaric aciduria type I
      • Neuroacanthocytosis
      • Systemic lupus erythematosus
      • Kernicterus
      • Antiphospholipid antibody syndrome
      • Mitochondrial encephalopathies

      Workup and Diagnosis

        • History
          –Fever, rash associated symptoms
          –History of streptococcal infections, rheumatic fever, arthritis
          –Birth history, family history, medications, ingestions
        • Physical exam
          –Eye exam: Kayser-Fleischer rings (Wilson disease)
          –Cardiac, joint, and skin exam (for rheumatic fever)
          –Neurologic exam should include eye movement, dysarthria, evaluation of tone, motor impersistence
      • Labs
        –Electrolytes, glucose, calcium, magnesium, LFTs, BUN/Cr, acetate, pyruvate
        –TSH, parathyroid hormone, hCG
        –CBC and blood smear (for acanthocytes)
        –Throat culture, antistreptolysin O titer
        –Ceruloplasmin (low in Wilson disease), amino acids
        –Lyme titer
        –Anti-nuclear, anti-cardiolipin, anti-phospholipid, anti dsDNA antibodies
        –Rheumatoid factor, lipid profile
        –Huntington disease genetic testing
        • Studies
          –Cardiac evaluation with Echo, ECG
          –LP useful in infectious or postinfectious cases
                –Multiple sclerosis (find oligoclonal bands)
          –Neuroimaging: CT or preferably MRI

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Facial Paralysis: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    Acquired

    • Bell palsy
      –A diagnosis of exclusion; 40% of cases
    • Acute otitis media
      –From erosion or dehiscence of facial canal
    • Chronic otitis media
      –Nerve compression from granulation tissue
      • Herpes zoster oticus
        –Often infects eighth nerve as well, with hearing loss and vertigo
    • Lyme disease
      –Usually several weeks after inoculation
      • Tumors
        –Temporal bone leukemia, rhabdomyosarcoma of head and neck
    • Melkersson-Rosenthal syndrome
      –Relapsing alternating facial paralysis
      –Recurrent facial edema
      –Fissured tongue
      • Temporal bone fracture
        –Although most cases involve longitudinal fractures, transverse may also result in hearing loss and vertigo
    • Facial wounds
      –Early repair if clean wound
      –Tag nerve for delayed repair if dirty wound
      • Iatrogenic
        –After otologic or parotid surgery

      Congenital
    • Traumatic (associated with prolonged and difficult labor)
    • Inherited disorders
      –Myotonic dystrophy: Progressive muscle weakness, facial paresis at birth
      –Albers-Schönberg disease: Osteopetrosis increases bone density, compresses nerve
      • Developmental abnormalities
        –Möbius syndrome: Facial paralysis with 6th cranial nerve palsy
        –Association with coloboma, heart defect, choanal atresia, genital hypoplasia, ear anomalies (CHARGE)
        –Goldenhar syndrome, also known as oculoauriculovertebral (OAV) syndrome: First and second branchial arch abnormalities
        –Asymmetric crying facies: Also called congenital unilateral lower lip palsy (CULLP)

      Workup and Diagnosis

        • History
          –Age of onset, rapid vs slow time-course, duration
          –Prior episodes, trauma, neurologic disorders, ear disease
      • Physical exam
        –Facial movement (e.g., while laughing, crying)
        –Facial symmetry at rest
        –Eye closure
        –Tear production, tongue papillae atrophy
        • Audiologic testing
          –Type of hearing loss predicts site of lesion (SNHL: internal auditory canal or CNS; CHL: middle ear)
      • Imaging studies
        –CT best for detecting pathology within temporal bone
        –MRI with gadolinium: Inflammation of nerve seen as enhancement on scan; predicts poorer outcome
        • Electrical testing
          –Objective means of monitoring function
          –Evoked electromyography (EEMG; electrically records muscle compound action potential; below 10% of normal side [i.e., 90% degeneration] predicts poor recovery; test must be done during first few days of paralysis)
          –Electromyography (EMG): Voluntary action potentials predict excellent prognosis; fibrillation potentials predict poor prognosis; polyphasic voluntary action potentials indicate reinnervation; test most useful weeks after injury

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Seizures – Childhood: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Febrile seizure
    • Cerebral dysgenesis: Disorders of neuronal migration, heterotopias, lissencephaly
    • Epilepsy syndromes
      –Childhood absence
      –Juvenile absence
      –Juvenile myoclonic epilepsy (JME)
      –Benign rolandic epilepsy (BRE)
    • Meningitis/encephalitis (e.g., HSV)
    • Cerebral abscess
    • Postinfectious (e.g., ADEM)
    • Hyponatremia
    • Hypernatremia
    • Hypocalcemia
    • Hypoglycemia
    • Toxins: Ingestions or sedative withdrawal
    • Trauma
    • Pyridoxine deficiency
    • Neoplasm
    • Degenerative
      –Alpers disease
      –Rett syndrome
      –Unterricht-Lundborg disease
      –Lafora disease
      –Neuronal ceroid lipofuscinosis
    • Genetic
      –Angelman syndrome
      –Aicardi syndrome
      • Metabolic
        –Medium chain acyl-CoA dehydrogenase deficiency (MCAD)
        –Myoclonus epilepsy and ragged-red fibers syndrome (MERRF)
        –Sialidosis
        –Glucose transporter deficiency
        –Urea cycle defects
    • Vascular: Stroke, hemorrhage, vasculitis
    • Hashimoto encephalitis
    • Seizure mimics
      –Breath-holding spells
      –Syncope, convulsive syncope
      –Gastroesophageal reflux
      –Cardiac arrhythmia
      –Movement disorder
      –Migraine
      –Benign paroxysmal vertigo
      –Parasomnia
      –Pseudo-seizure
      –Rage attack

    Workup and Diagnosis

    • History: Detailed description of the spell, loss of consciousness, eye deviation, time of onset, other suspicious spells (jerking, staring, day-dreaming), birth and developmental history, previous history of head trauma, encephalitis, febrile seizures, medications at home, recent infections
    • Physical exam: Dysmorphic features, skin rash, retinal exam for cherry-red spot, macular degeneration, hepatosplenomegaly, meningismus
    • Full neurologic examination: Postictal weakness can provide clues to the focus of seizures (Todd paralysis)
    • Labs: Glucose, electrolytes, calcium, toxicology screen, ammonia, lactate, pyruvate, genetic testing for specific disorders (MECP2 mutation for Rett, FISH on chromosome 15 for Angelman)
    • Lumbar puncture to rule out infection (including HSV PCR), glucose transporter deficiency
      • EEG can help make the diagnosis of focal vs generalized epilepsy
        –Crucial for decisions of treatment choices
    • MRI can help determine any structural abnormalities, including cerebral dysgenesis, abscess, neoplasm, temporal lobe sclerosis
    • For other specific etiologies, one can follow up with skin biopsy, CSF amino acids, biotinidase level, TSH, anti-thyroglobulin antibodies, rheumatologic workup

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Seizures – Neonatal: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Hypoxic ishemic encephalopathy
    • Bacterial meningitis/sepsis
    • Stroke
    • Cerebral dysgenesis
    • Electrolyte disturbances
      –Hypoglycemia
      –Hyponatremia
      –Hypomagnesemia
      –Hypocalcemia
    • Maternal drug use
      –Drug withdrawal after delivery
      –Direct effect of drugs, such as cocaine
    • Congenital infections (TORCH)
      –Toxoplasmosis
      –Syphilis
      –Rubella
      –CMV
      –HSV
    • HSV encephalitis
      • Intracranial hemorrhage
        –Subdural hemorrhage
        –Intraparenchymal hemorrhage
        –Intraventricular hemorrhage in the premature infant
        –Subarachnoid hemorrhage
    • Urea cycle disturbances
    • Smith-Lemli-Opitz syndrome
    • Nonketotic hyperglycinemia
    • Pyridoxine deficiency
    • Fructose dysmetabolism
    • Amino acidurias
      –Maple syrup urine disease
      –Proprionic acidemia
    • Molybdenum cofactor deficiency
    • Mitochondrial encephalopathy
    • Glucose transporter deficiency
      • Benign etiologies
        –Benign idiopathic neonatal seizures (fifth day fits)
        –Benign familial neonatal seizures
    • Movements commonly mistaken for seizures
      –Benign neonatal sleep myoclonus
      –Jitteriness (may be secondary to hypoglycemia, drug withdrawal, or idiopathic)
      –Gastroesophageal reflux (arching, writhing)
      –Breath-holding spell

    Workup and Diagnosis

    • History: Previous pregnancies, fetal movements, infections, blood pressure problems during pregnancy, maternal drug/medication use, family history, Apgar scores, nuchal cord, birth weight, feeding problems, association of the spells to feeding and sleep
    • Physical exam
      –Deformities, dermatoglyphics, skin lesions, hepatosplenomegaly, funduscopic exam, corneal opacities
      –Mental status: Spontaneous level of activity of the infant; responsiveness to light, sound, and touch
      –Muscle tone: Passive manipulation of limbs
      –Primary neonatal reflexes (Moro, palmar grasp, tonic neck response) and muscle stretch reflexes
    • Labs: Glucose, electrolytes, lactate, liver function tests, ammonia, TORCH titers, pyruvate, chromosomes, 17-hydroxycorticosteroid, serum amino acids, copper
    • Neuroimaging: CT or MRI
    • Lumbar puncture for meningitis and encephalitis, including HSV, glucose transporter deficiency, nonketotic hyperglycinemia
    • EEG: Critical in making the diagnosis of seizures in the newborn; monitoring of the child during one of the spells is the best way to make the diagnosis of seizures
    • If gastroesophageal reflux is suspected, pH/thermistor monitoring is helpful to document a temporal relation

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    TREMOR AND OTHER INVOLUNTARY MOVEMENTS: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The workup of tremor and other involuntary movements involves most of all a good history. The neurologic exam is important as it will determine the type of tremor. Rapid fine tremors (8–20/s) are suggestive of hyperthyroidism and emotional disorders. Coarser tremors at rest suggest parkinsonism, whereas a flapping tremor of 4 to 8 per second suggests Wilson disease. The association of other neurologic signs helps pin down the diagnosis. Spasms of pain suggest a thalamic syndrome, whereas ataxia suggests Friedreich ataxia and loss of memory suggests manganese toxicity. Laboratory tests will be useful in selected cases. Blood lead, manganese, copper, and ceruloplasmin levels may be necessary. A T3, T4, and FT4 index will confirm the diagnosis of Graves disease. Other tests that may be helpful may be found in the Appendix or listed below.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    FACIAL PARALYSIS: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The clinical picture will frequently help determine the cause of facial paralysis. Peripheral facial palsy as occurs in Bell palsy involves the forehead muscles and there is difficulty in closing the eyelid, whereas central facial palsy involves the face and lips and there is often associated hemiplegia or monoplegia. When there is exclusively a peripheral facial palsy without hearing loss or other neurologic signs, Bell palsy should be strongly suspected, although diabetes and myasthenia gravis need to be excluded. A bilateral peripheral nerve palsy should make one consider Guillain–Barré syndrome and be on the look out for paralysis of the extremities as well. Bilateral facial palsy is also seen in myotonic dystrophy and myasthenia gravis. A “Bell palsy” with hearing loss and an aural discharge should prompt consideration of mastoiditis and petrositis. If there is hearing loss without a discharge, the possibility of an acoustic neuroma or cholesteatoma must be entertained. The association of a central facial palsy with hemiplegia brings up a host of possibilities including subdural hematoma, brain abscess, brain tumor, and cerebrovascular accident. The workup of these conditions is considered on page 545.

    If the patient has clinical Bell palsy, one could start a therapy without a workup, but it is wise to get an x-ray of the skull and mastoids to rule out mastoiditis and petrositis and a glucose tolerance test to rule out diabetes. An acetylcholine receptor antibody titer or Tensilon test would only be ordered if the palsy were intermittent or there was other cranial nerve signs. If a middle ear infection or acoustic neuroma is suspected, the patient needs x-ray of the mastoids and petrous bones and a CT scan or MRI of the brain and auditory canal.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    WEAKNESS OR PARALYSIS OF ONE OR MORE EXTREMITIES: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The site of weakness is determined by associated symptoms and signs. Fasciculations suggest nerve root or anterior horn cell involvement, whereas sensory changes suggest peripheral nerve or spinal cord involvement. A combination of spasticity in the lower extremities and flaccid and atrophic weakness in the upper extremities suggests cervical cord involvement. Cranial nerve lesions in association with paraplegia or quadriplegia usually indicate a brainstem lesion.

    The workup will depend on the site in which the pathology is suspected to be located. If muscle is the site, then an EMG or biopsy is indicated. If the myoneural junction is involved a Tensilon test is done. Peripheral nerve lesions require a more extensive workup, including a glucose tolerance test, blood lead level, urine for porphobilinogens, EMG, NCV, and possibly a muscle biopsy. Spinal cord lesions may require x-ray of the spine, CT scan or MRI, myelography, diskography, and spinal fluid analysis. Brainstem and cerebral lesions are best screened with a skull x-ray, MRI, or CT scan before a spinal tap or arteriogram is considered.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    LYMPHADENOPATHY, GENERALIZED: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Obviously, it is tempting simply to do a lymph node biopsy, but certain other procedures should be done first. If the patient is febrile, febrile agglutinins, Monospot test, blood cultures, and cultures of any other suspicious body fluid should be made. An FTA-ABS test should be done as well as a chest x-ray and tuberculin test to rule out tuberculosis. A blood count usually shows leukemia, but a bone marrow may be necessary to diagnose leukemia, Hodgkin disease, and the reticuloendothelioses. Other x-rays, skin tests, and special diagnostic procedures may be necessary.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    WEAKNESS AND FATIGUE, GENERALIZED: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The association of other symptoms and signs with generalized weakness and fatigue is very important in pinning down a diagnosis. Generalized lymphadenopathy and fatigue suggest infectious mononucleosis, lymphoma, or tuberculosis or other chronic infection such as AIDS. Weakness and weight loss and polyphagia with polyuria and polydypsia would suggest hyperthyroidism or diabetes mellitus. Generalized weakness with polyuria and no significant weight loss suggests hyperparathyroidism. Weakness with pallor suggests some type of anemia. Weakness and weight loss without polyuria or polyphagia suggest malignancy or malabsorption syndrome. Weakness with other significant neurologic signs and symptoms prompts the consideration of muscular dystrophy, amyotrophic lateral sclerosis, or multiple sclerosis. Weakness with drug or alcohol use prompts the investigation of drug or alcohol abuse. Caffeine, especially in large quantities, can also cause significant weakness and chronic fatigue.

    The initial workup of weakness and fatigue requires a CBC, sedimentation rate, drug screen, chemistry panel, thyroid profile, ANA, chest x-ray and ECG. If muscular dystrophy or dermatomyositis is suspected, urine for creatinine, creatine and myoglobin can be done. Ultimately, a muscle biopsy may be indicated. If myasthenia gravis is suspected, serum for acetylcholine receptor antibody may be done. If Addison disease is suspected, a serum cortisol may be done. A 24-hour urine aldosterone level may be done to exclude primary aldosteronism. Serum PTH may be done to exclude hyperparathyroidism.

    It would be wise to consult an infectious disease specialist before ordering an expensive workup. It would also be wise to consult an oncologist when searching for a malignancy before ordering an expensive workup.

    When all tests have negative findings, many clinicians have been tempted to make a diagnosis of chronic fatigue syndrome. It is questionable whether this is truly a disease or not.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    Aura: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Carpopedal spasm: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient isn't in distress, obtain a detailed history. Ask about the onset and duration of the spasms and ask for a description of pain they produce. Also ask about related signs and symptoms of hypocalcemia, such as numbness and tingling of the fingertips and feet, other muscle cramps or spasms, and nausea, vomiting, and abdominal pain. Check for previous neck surgery, calcium or magnesium deficiency, tetanus exposure, and hypoparathyroidism.

    During the history, form a general impression of the patient's mental status and behavior. If possible, ask family members or friends if they've noticed changes in the patient's behavior. Mental confusion or even personality changes may occur with hypocalcemia.

    Inspect the patient's skin and fingernails, noting dryness or scaling and ridged, brittle nails.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Level of consciousness, decreased: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

    Because a decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Myoclonus: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient is stable, evaluate his level of consciousness (LOC) and mental status. Ask about the frequency, severity, location, and circumstances of myoclonus. Has he ever had a seizure? If so, did myoclonus precede it? Is myoclonus ever precipitated by a sensory stimulus? During the physical examination, check for muscle rigidity and wasting, and test deep tendon reflexes.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Paralysis: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or recent injury. Explore related signs and symptoms, noting fevers, headaches, vision disturbances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

    Next, perform a complete neurologic examination, testing cranial nerve (CN), motor, and sensory function and deep tendon reflexes (DTRs). Assess strength in all major muscle groups, and note muscle atrophy. (See Testing muscle strength, pages 418 and 419.) Document all findings to serve as a baseline.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Seizures, complex partial: History
    (Handbook of Signs & Symptoms (Third Edition))

    If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don’t approach him if he’s angry or violent.) Calmly encourage him to sit down, and remain with him until he’s fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Seizures, generalized tonic-clonic: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If you didn’t witness the seizure, obtain a description from the patient’s companion. Ask when the seizure started and how long it lasted. Did the patient report unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body right away? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have other seizures before recovering?

    If the patient may have sustained a head injury, observe him closely for loss of consciousness, unequal or nonreactive pupils, and focal neurologic signs. Does he complain of a headache and muscle soreness? Is he increasingly difficult to arouse when you check on him at 20-minute intervals? Examine his arms, legs, and face (including tongue) for injury, residual paralysis, or limb weakness.

    Next, obtain a history. Has the patient ever had generalized or focal seizures before? If so, do they occur frequently? Do other family members also have them? Is the patient receiving drug therapy? Is he compliant? Also, ask about sleep deprivation and emotional or physical stress at the time the seizure occurred.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Seizures, simple partial: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Make sure to record the patient’s seizure activity in detail; your data may be critical in locating the lesion in the brain. Does the patient turn his head and eyes? If so, to what side? Where does movement first start? Does it spread? Because a partial seizure may become generalized, you’ll need to watch closely for loss of consciousness, bilateral tonicity and clonicity, cyanosis, tongue biting, and urinary incontinence. (See “Seizures, generalized tonic-clonic,” page 554.)

    After the seizure, ask the patient to describe exactly what he remembers, if anything, about the seizure. Check the patient’s LOC, and test for residual deficits (such as weakness in the involved extremity) and sensory disturbances.

    Then obtain a history. Ask the patient what happened before the seizure. Can he describe an aura or did he recognize its onset? If so, how — by a smell, a visual disturbance, or a sound or visceral phenomenon such as an unusual sensation in his stomach? How does this seizure compare with others he has had?

    Also, explore fully any history — recent or remote — of head trauma. Check for a history of stroke or recent infection, especially with a fever, headache, or stiff neck.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Seizures, absence: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If you suspect a patient is having an absence seizure, evaluate its occurrence and duration by reciting a series of numbers and then asking him to repeat them after the attack ends. If the patient has had an absence seizure, he can’t do this. Alternatively, if the seizures are occurring within minutes of each other, ask the patient to count for about 5 minutes. He’ll stop counting during a seizure and resume when it’s over. Look for accompanying automatisms. Find out if the family has noticed a change in behavior or deteriorating schoolwork.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Vocal cord paralysis: Diagnosis
    (Professional Guide to Diseases (Eighth Edition))

    The patient history and characteristic features suggest vocal cord paralysis.

    CONFIRMING DIAGNOSIS Visualization by indirect laryngoscopy shows one or both cords fixed in an adducted or partially abducted position and confirms the diagnosis.

    X-ray or computed tomography scan detect abnormalities in the mediastinum that may be responsible for the injury.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Diseases (Eighth Edition), 2005

    Aura: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    After providing emergency care, obtain a thorough history of the patient’s headaches or seizures, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Carpopedal spasm: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient isn’t in distress, obtain a detailed history. Ask about the onset and duration of the spasms and the degree of pain they produce. Also ask about related signs and symptoms of hypocalcemia, such as numbness and tingling of the fingertips and feet, other muscle cramps or spasms, and nausea, vomiting, and abdominal pain. Check for previous neck surgery, calcium or magnesium deficiency, tetanus exposure, and hypoparathyroidism.

    During the history, form a general impression of the patient’s mental status and behavior. If possible, ask family members or friends if they’ve noticed changes in the patient’s behavior because hypocalcemia can cause confusion and even personality changes.

    Inspect the patient’s skin and fingernails, noting any dryness or scaling and ridged, brittle nails.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Level of consciousness, decreased: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

    Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Myoclonus: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient is stable, evaluate level of consciousness and mental status. Ask about the frequency, severity, location, and circumstances of the myoclonus. Has he ever had a seizure? If so, did myoclonus precede it? Is the myoclonus ever precipitated by a sensory stimulus? During the physical examination, check for muscle rigidity and wasting, and test deep tendon reflexes.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Paralysis: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or recent injury. Explore related signs and symptoms, noting fever, headache, vision disturbances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

    Next, perform a complete neurologic examination, testing cranial nerve, motor, and sensory function and deep tendon reflexes. Assess strength in all major muscle groups, and note any muscle atrophy. (See Testing muscle strength, pages 530 and 531.) Document all findings to serve as a baseline.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Seizures, complex partial: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don’t approach him if he’s angry or violent.) Calmly encourage him to sit down, and remain with him until he’s fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Seizures, generalized tonic-clonic: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If you didn’t witness the seizure, obtain a description from the patient’s companion. Ask when the seizure started and how long it lasted. Did the patient report any unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body right away? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have any other seizures before recovering?

    If the patient may have sustained a head injury, observe him closely for loss of consciousness, unequal or nonreactive pupils, and focal neurologic signs. Does he complain of headache and muscle soreness? Is he increasingly difficult to arouse when you check on him at 20-minute intervals? Examine his arms, legs, and face (including tongue) for injury, residual paralysis, or limb weakness.

    Next, obtain a history. Has the patient ever had generalized or focal seizures before? If so, do they occur frequently? Do other family members also have them? Is the patient receiving drug therapy? Is he compliant? Ask about sleep deprivation and emotional or physical stress at the time the seizure occurred.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Seizures, simple partial: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Be sure to record the patient’s seizure activity in detail; your data may be critical in locating the lesion in the brain. Does the patient turn his head and eyes? If so, to what side? Where does movement first start? Does it spread? Because a partial seizure may become generalized, you’ll need to watch closely for loss of consciousness, bilateral tonicity and clonicity, cyanosis, tongue biting, and urinary incontinence. (See “Seizures, generalized tonic-clonic,” page 708.)

    After the seizure, ask the patient to describe exactly what he remembers, if anything, about the seizure. Check the patient’s LOC, and test for residual deficits (such as weakness in the involved extremity) and sensory disturbances.

    Then obtain a history. Ask the patient what happened before the seizure. Can he describe an aura or did he recognize its onset? If so, how—by a smell, a visual disturbance, or a sound or visceral phenomenon, such as an unusual sensation in his stomach? How does this seizure compare with others he has had?

    Explore fully any history, recent or remote, of head trauma. Check for a history of stroke or recent infection, especially with fever, headache, or a stiff neck.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Chorea [Choreiform movements]: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Ask the patient and his family when they first noticed the choreiform movements. Do the movements disappear when the patient is asleep? Find out if anyone in the patient’s family exhibits the same type of movements, and ask about a family history of such diseases as Huntington’s disease. Also ask which medications the patient is taking. Obtain an occupational history, noting especially prolonged exposure to manganese or other metals. As you obtain the history, observe the patient for excessive restlessness and periodic facial grimaces that may interrupt his speech.

    Perform a physical examination to evaluate the severity of the patient’s chorea. Ask him to stick out his tongue and keep it out. Typically, he’ll be unable to do this; instead, his tongue will dart in and out of his mouth. Observe the patient’s arms and legs separately for involuntary jerky movements. Ask him to extend and flex his hand as if halting traffic; the choreiform movements will be extremely evident in this position. Also, check for such related signs as athetosis, rigidity, or tremor.

    To assess the patient for choreoathetotic gait, ask him to walk. He may change the position of his trunk and upper body parts with each step and jerk and tilt his head to one side. Because of superimposed involuntary movements and postures, the patient’s legs may move slowly and awkwardly. (An involuntary movement suspending his leg momentarily with each step may give a dancing quality to his gait.)

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Seizures, absence: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If you suspect a patient is having an absence seizure, evaluate its occurrence and duration by reciting a series of numbers and then asking him to repeat them after the attack ends. If the patient has had an absence seizure, he’ll be unable to do this. Alternatively, if the seizures are occurring within minutes of each other, ask the patient to count for about 5 minutes. He’ll stop counting during a seizure and resume when it’s over. Look for accompanying automatisms. Find out if the family has noticed a change in behavior or deteriorating schoolwork.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Seizures: History.
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

    Seizures can be confused with migraines and syncope.

    A. Characteristics of the seizure

    1. What was witnessed? Does the patient fall? Is there urinary or fecal incontinence, tongue biting, or loss of consciousness? Is there a postictal period? Is there staring, lip smacking, or automatisms? Seizure activity in neonates may present with subtle activities such as apnea, tremors, grimacing, or spasms.

     2. What can the patient remember? Are there associated sensations (odors, lights, emotions, tactile input)? Is there an aura?

     3. At what age was seizure onset? What is the frequency of the spells?

    4. What is the setting? Is there evidence supporting anoxia or hypoxia? Was there a sudden rise in temperature (4)? Did the seizure follow flashing lights, exercise, sleeplessness, fasting, or menses?

    5. Red flags include adult age at onset, changing pattern, and regression of motor skills.

     B. Chronology of the seizure. Most seizures present a characteristic pattern. A pattern of change or worsening of seizures can indicate new causation.

     C. Family history. Febrile, myoclonic, primary idiopathic seizures, and genetic syndromes with seizures often present a familial pattern.

     D. Psychosocial aspects. Ask how the family, teachers, employers interact with the patient.

     E. Other information. Important data include use of alcohol or drugs, medications that lower seizure threshold, toxic occupational or recreational chemicals, and severe physical [previous head trauma, central nervous system (CNS) infection, chronic illness] or psychosocial stressors.

    Physical examination (PE)

    A. Focused neurologic examination. Examine level of consciousness, pupils, fundi, cranial nerves, reflexes, gait, muscle strength, general sensory, coordination, and Romberg’s sign (4). Look for abnormal motor activity and test for abnormal reflexes.

    B. Additional PE

     1. Look for signs of systemic illness: cardiac disease (cyanosis, pallor, irregular rhythm, cool extremities) and chronic alcoholism (ascites, jaundice, caput medusae, and bruising).

     2. Look for residual signs of trauma or limb asymmetry.

    3. Look for dysmorphic manifestations of heritable disease: vascular malformations (Sturge–Weber), adenoma sebaceum (tuberous sclerosis), or café au lait spots and subcutaneous nodules (neurofibromatosis).

    4. Gingival hypertrophy suggests phenytoin therapy.

    » READ BOOK EXCERPT ONLINE »

    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Lymphadenopathy, Generalized: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

     should focus on those common causes of generalized lymphadenopathy.

     A. History of present illness should focus on the duration, location, quality, and context of the lymphadenopathy. Note associated signs and symptoms such as rash, fever, sore throat, and cough (4) (Chapters 2.6, 8.1, and 13.6). The goal is to ascertain if the adenopathy is attributable to a specific cause.

     B. Past medical history should focus on known illness, medication usage, and allergies. Serum sickness from antibiotic use as well as diphenylhydantoin for seizure prevention can cause generalized lymphadenopathy. Common chronic illnesses (e.g., lupus erythematosus and rheumatoid arthritis) can also cause generalized lymphadenopathy.

     C. Social history should focus on the patient’s occupation, sexual history, and alcohol use. Hepatitis B, secondary syphilis, and early human immunodeficiency virus (HIV) can all present with generalized lymphadenopathy. Patients with Hodgkin’s disease can develop painful adenopathy with alcohol use.

    D. Family history. Inquire about family illness with a genetic predisposition as well as any exposures to household contacts with infectious diseases (e.g., tuberculosis, infectious mononucleosis, or hepatitis B).

     E. Review of systems should focus on constitutional symptoms such as weight loss, fatigue, night sweats, malaise, arthralgias, nausea, and vomiting (1).

    Physical examination

     A. General. A comprehensive physical examination should be performed on all patients with generalized lymphadenopathy. Focus on those findings consistent with the most frequent causes of generalized lymphadenopathy. Note the patient’s temperature and weight, because fever and weight loss are frequent findings. Examine the skin, mucous membranes, abdominal organs, and joints; specifically, the presence of rash, mucocutaneous ulceration, organomegaly, and arthritis can be a guide to possible causes of the adenopathy. The presence of splenomegaly in a patient with adenopathy implies a systemic illness (e.g., infectious mononucleosis, lymphoma, leukemia, lupus, sarcoidosis, toxoplasmosis, or cat scratch disease) (Chapter 15.4). Additionally, search for other abnormal lymph nodes. Studies have shown that clinicians identified only 17% of those cases of generalized lymphadenopathy when it was present (1).

     B. Nodal examination. The abnormal lymph node groups should be specifically examined.

    1. Size. Lymph nodes enlarged up to 1 cm in diameter can be considered normal in size. These have a low malignancy risk and can usually be observed. Lymph nodes greater than 1.5 cm × 1.5 cm in area have been shown to have a 38% risk of cancer involvement and merit further workup (2).

     2. Location. Anterior cervical, submandibular, and inguinal nodes are normally palpable. The presence of supraclavicular adenopathy is always abnormal and carries a 90% cancer risk in those aged more than 40 years. Postocciptal nodes are associated with infectious mononucleosis, scalp lesions, toxoplasmosis, and non-Hodgkin’s lymphoma. Axillary nodes are associated with upper extremity infections, breast cancer, cat scratch disease, and lymphomas. Epitrochlear nodes are associated with pyogenic infections, sarcoidosis, tularemia, and syphilis. Inguinal nodes are associated with lower extremity infections and sexually transmitted diseases.

     3. Pain. The presence or absence of pain is not a reliable indicator of the cause of adenopathy. Capsular swelling from acute infections can cause pain as can necrotic hemorrhage from a malignant lymph node.

     4. Consistency. Rock hard nodes are consistent with metastatic disease (2). Firm rubbery nodes are found with lymphomas. Soft nodes tend to occur with infectious causes; however, this should not be considered diagnostic.

    » READ BOOK EXCERPT ONLINE »

    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Seizures: Differential Overview

    (Field Guide to Bedside Diagnosis)

    ❑ Generalized (grand mal)

    ❑ Partial (focal)

    ❑ Complex partial (temporal lobe)

    ❑ Absence (petit mal)

    ❑ Vasovagal syncope

    ❑ Myoclonic

    ❑ Akinetic (drop attacks)

    ❑ Psychomotor

    ❑ Pseudoseizures

    Diagnostic Approach

    When the patient is found unresponsive, the differential is seizure versus syncope. Interviewing witnesses is crucial to ascertain the diagnosis. Seizures can be distinguished by color (cyanosis in seizure, pallor in syncope), aura, injury from falling, protracted tonic-clonic activity, tongue biting, urinary incontinence, and slow recovery of consciousness (seizure). Confusion, headache, and drowsiness are sequelae of seizure, whereas physical weakness and a clear sensorium occur with syncope. Seizures often have a promontory aura, such as an odor, and syncope has a prodrome of tunnel vision. Seizures are followed by eye closure, rotation of the head side-to-side, and prolonged, motionless unresponsiveness.

    General precipitating factors include sleep deprivation, systemic disease such as renal failure, metabolic/electrolyte disorder such as hypoglycemia or hyponatremia, alcohol use, or drug use. Elicit a history of febrile seizures or prior head trauma. Common causes of recurrent seizures in previously controlled patients include alcohol use, intercurrent infection, and missed medication doses.

    A neurological examination will indicate whether there is an underlying structural problem as evidenced by mild hemiparesis, reflex asymmetry, or extensor plantar response. Seizures are more common in slowly growing cerebral lesions, such as low-grade glioma or meningioma.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

    Vocal cord paralysis: Diagnosis
    (Handbook of Diseases)

    Patient history and characteristic features suggest vocal cord paralysis. Visualization by indirect laryngoscopy shows one or both cords fixed in an adducted or partially adducted position and confirms the diagnosis.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Diseases, 2003

    Carpopedal spasm: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Ask the patient about the onset and duration of the spasms and the degree of pain they produce. Assess him for related signs and symptoms of hypocalcemia, such as numbness and tingling of the hands and feet, other muscle cramps or spasms, and nausea, vomiting, and abdominal pain. Determine whether the patient’s history includes previous neck surgery, calcium or magnesium deficiency, tetanus exposure, or hypoparathyroidism.

    Ask the patient’s family members whether they noticed changes in his behavior. Mental confusion — even personality changes — may occur with hypocalcemia.

    Physical examination

    Inspect the patient’s skin and fingernails, noting dryness or scaling and ridged, brittle nails. Obtain his vital signs. Perform a head-to-toe assessment with a complete respiratory assessment. Check Chvostek’s sign (tapping of the facial nerve, which results in facial nerve spasm).

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Level of consciousness, decreased: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

    Physical examination

    Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms. Perform a complete neurologic assessment and a physical assessment. Determine the patient’s baseline Glasgow Coma Scale score and evaluate on an ongoing basis.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Myoclonus: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    If the patient is stable, evaluate his level of consciousness and mental status. Ask about the frequency, severity, location, and circumstances of the myoclonus. Has he ever had a seizure? If so, did myoclonus precede it? Is the myoclonus ever precipitated by a sensory stimulus? 

    Physical examination

    During the physical examination, check for muscle rigidity and wasting, and test deep tendon reflexes. Evaluate level of consciousness and mental condition. Perform a complete neurologic and musculoskeletal assessment.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Paralysis: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or injury. Explore related signs and symptoms, noting fever, headache, vision disturbances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

    Physical examination

    Perform a complete neurologic examination, testing cranial nerve, motor, and sensory function and deep tendon reflexes (DTRs). Assess strength in all major muscle groups, and note muscle atrophy. (See Testing muscle strength, pages 230 and 231.) Document all findings to serve as a baseline.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Seizures, generalized tonic-clonic: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Obtain the patient’s medical history. Has he had generalized or focal seizures before? If so, how frequently? Do other family members have seizures? Is the patient receiving drug therapy? Is he compliant? Ask about sleep deprivation and emotional or physical stress at the time the seizure occurred. Ask about the use of alcohol or illicit drugs.

    If you didn’t witness the seizure, obtain a description from the patient’s family. Ask when it started and how long it lasted. Did the patient report unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body immediately? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have other seizures before recovering? Does he complain of headache and muscle soreness?

    Physical examination

    If the patient may have sustained a head injury, perform a complete neurologic examination, observing closely for loss of consciousness, unequal or nonreactive pupils, and focal neurologic signs. Assess his vital signs. Is he increasingly difficult to arouse when you check on him at 20-minute intervals? Examine his arms, legs, and face (including tongue) for injury, residual paralysis, or limb weakness.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Aura: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Carpopedal spasm: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient isn’t in distress, obtain a detailed history. Ask about the onset and duration of the spasms and the degree of pain they produce. Also ask about related signs and symptoms of hypocalcemia, such as numbness and tingling of the fingertips and feet, other muscle cramps or spasms, and nausea, vomiting, and abdominal pain. Check for previous neck surgery, calcium or magnesium deficiency, tetanus exposure, and hypoparathyroidism. Ask the patient if he had recent puncture wounds, and inquire about his immunizations.

    During the history, form a general impression of the patient’s mental status and behavior. If possible, ask family members or friends if they have noticed changes in the patient’s behavior. Mental confusion or even personality changes may occur with hypocalcemia.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Chorea: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Ask the patient and his family when they first noticed the choreiform movements. Do the movements disappear when the patient is asleep? Find out if anyone in the patient’s family exhibits the same type of movements, and ask about a family history of such diseases as Huntington’s disease. Also ask which medications the patient is taking. Obtain an occupational history, noting especially prolonged exposure to manganese or other metals. As you obtain history information, observe the patient for excessive restlessness and periodic facial grimaces that may interrupt his speech.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Level of consciousness, decreased: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease or cancer; recent trauma or infection; drug and alcohol use; and the development of other signs and symptoms.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Myoclonus: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient is stable, evaluate level of consciousness (LOC) and mental status. Ask about the frequency, severity, location, and circumstances of myoclonus. Has he ever had a seizure? If so, did myoclonus precede it? Is the myoclonus ever precipitated by a sensory stimulus?

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Paralysis: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information, if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or recent injury. Explore related signs and symptoms, noting fever, headache, vision disturbances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Seizures, complex partial: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don’t approach him if he’s angry or violent.) Calmly encourage him to sit down, and remain with him until he’s fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Seizures, generalized tonic-clonic: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If you didn’t witness the seizure, obtain a description from the patient’s companion. Ask when the seizure started and how long it lasted. Did the patient report any unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body right away? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have any other seizures before recovering? Does he complain of headache and muscle soreness? Is he increasingly difficult to arouse when you check on him at 20-minute intervals?

    Next, obtain a history. Has the patient ever had generalized or focal seizures before? If so, do they occur frequently? Do other family members also have them? Is the patient receiving drug therapy? Is he compliant? Also, ask about sleep deprivation and emotional or physical stress at the time the seizure occurred.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Seizures, simple partial: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Record the patient’s seizure activity in detail; your data may be critical in locating the lesion in the brain. Does the patient turn his head and eyes? If so, to what side? Where does movement first start? Does it spread? Because a partial seizure may become generalized, you’ll need to watch closely for loss of consciousness, bilateral tonicity and clonicity, cyanosis, tongue biting, and urinary incontinence. (See “Seizures, generalized tonic-clonic,” page 598.)

    After the seizure, ask the patient to describe exactly what he remembers, if anything, about the seizure. Then obtain a history. Ask the patient what happened before the seizure. Can he describe an aura or did he recognize its onset? If so, how — by a smell, a visual disturbance, or a sound or visceral phenomenon, such as an unusual sensation in his stomach? How does this seizure compare with others he has had?

    Also, explore fully any history, recent or remote, of head trauma. Check for a history of stroke or recent infection, especially with fever, headache, or a stiff neck.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Seizures: Clinical Features and Diagnosis
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Febrile Seizures

  • Can be definedas a seizure occurring in child <6 yrs of age associatedwith a temperature >38°C without evidence of intracranialinfection or acute systemic metabolic disorder. These seizures areuncommon before 6 mos of age.
  • Can be categorized as simple or complex.Most febrile seizures are simple and consist of single, brief, generalizedseizures with tonic-clonic or clonic movements lasting several minutes,although they can last as long as 15 mins. If they occur in a series,duration is <30 mins. Complex febrile seizures last >15mins, can occur in a prolonged series for several hours, and maybe focal.
  • Common clinical dilemma, especiallyin infants, is whether febrile seizure could indicate presence ofmeningitis or encephalitis. Lumbar puncture should be performedif these infections are suspected. This is especially importantin infants <18 mos of age, when physical exam is not asreliable as in older children.

    • Hypoxic-Ischemic Encephalopathy

  • Most commoncause of neonatal seizures is hypoxic-ischemic encephalopathy.
  • In most cases asphyxia occurs beforeor during delivery. History of toxemia, abruptio placenta, cordprolapse, fetal bradycardia, meconium staining, or prolonged failureto establish spontaneous respiration can be presumptive evidenceof intrauterine hypoxia.
  • In infants and children, hypoxic-ischemicencephalopathy may occur from suffocation, near drowning, shock,and cardiorespiratory arrest from any cause.

    • Brain Disorders

    Cerebral Malformations

    Seizures may arise from malformations ofthe brain. Some examples are polymicrogyria, holoprosencephaly,and cortical heterotopias. MRI is diagnostic.

    Intracranial Infection

    Infections (e.g., bacterial meningitis, encephalitis,and brain abscess) may be associated with seizures. See Chap. 3, Alteration in Consciousness.

    Intracranial Hemorrhage

  • Hypoxiais major factor in development of intraventricular hemorrhage inpreterm infants, whereas subarachnoid hemorrhage usually occursas result of difficult labor or delivery in near-term infants.
  • In infants and children, head traumais most common cause of intracranial hemorrhage.
  • Head U/S, CT, and MRI areuseful in localizing and defining extent of hemorrhage. Study performeddepends on age of child and clinical circumstances. ≥1 modalitymay be necessary.

    • Other

    Brain tumors, cerebrovascular disorders,neurocutaneous disorders, and neurodegenerative diseases also maycause seizures. See Chap. 3,Alteration in Consciousness; Chap. 13, Developmental Delay;and Chap. 25, Headache.

    Hypertensive Encephalopathy

  • Severe generalizedheadache and visual disturbances (e.g., blurring of vision) maybe symptoms of severe hypertension.
  • Seizures also may occur; however, itis impossible to predict at what BP level seizures will occur.
  • BP should be measured in every individualwho has a seizure (see Chap.32, Hypertension).

    • Drugs and Toxins

  • Ingestionof the following substances may produce seizures: theophylline,phenothiazines, tricyclic antidepressants, camphor, glutethimide,benzene, acetylsalicylic acid, morphine, codeine, cocaine, heroin,amphetamines, and lead.
  • History and physical exam may be diagnostic.
  • Urine or serum level of implicateddrug, chemical, or heavy metal confirms diagnosis.

    • Metabolic Disorders

    Hypoglycemia

  • Can be definedas blood glucose concentration of <40 mg/dL afterinitial 2–3 hrs of life.
  • Clinical manifestations of hypoglycemiain the neonate include jitteriness, tremors, lethargy, poor feeding,apnea, seizures, and alteration of consciousness. In infancy andchildhood, clinical findings include anxiety, hunger, headache,vomiting, sweating, fatigue, lassitude, seizures, and alterationof consciousness.

    • Principal Causes of Hypoglycemia

    1. Transientneonatal hypoglycemia
      1. Associated with decreased substrate or enzymefunction
      2. Associated with hyperinsulinemia
    2. Persistent hypoglycemia in infants,children, or adolescents
      1. Hyperinsulinemia
      2. Hormone deficiency
      3. Ketotic hypoglycemia
      4. Drugs or toxins
        1. Insulin
        2. Salicylates
        3. Propranolol
        4. Alcohol
        5. Oral hypoglycemic agents
      5. Hepatic disease
        1. Hepatitis
        2. Cirrhosis
        3. Reye syndrome
    3. Metabolic disorders
      1. Glycogenstorage diseases (types O, I, III,VI)
      2. Disorders of gluconeogenesis
      3. Galactosemia
      4. Hereditary fructose intolerance
      5. Maple syrup urine disease
      6. Tyrosinemia
      7. Propionic acidemia
      8. Methylmalonic acidemia
      9. Medium-chain acyl-CoA dehydrogenasedeficiency
    4. Systemic disorders
      1. Septicemia
      2. Malnutrition
      3. Malabsorption
      4. Burns
      5. Shock

    Transient Neonatal Hypoglycemia

  • Transienthypoglycemia may occur in neonates because of inadequate substrate(liver glycogen, muscle protein, body fat) or lack of fully developedenzyme systems to sustain glucose production.
  • Most common in infants who are premature,small for gestational age, or the smaller of twins, but it alsocan occur in infants born to toxemic mothers and infants who experiencesevere respiratory distress.
  • Maternal diabetes mellitus and perinatalasphyxia are most common causes of transient neonatal hyperinsulinemia.
  • Resolution of hypoglycemia usuallyoccurs in 2–3 days with milk feedings or infusion of intravenousglucose.

    • Persistent Hypoglycemia in Infants, Children, or Adolescents

    Hyperinsulinemia

  • Most commoncause of persistent hypoglycemia in infancy is hyperinsulinism,which can occur from birth to 18 mos of age.
  • It should be suspected in a macrosomicinfant with severe nonketotic hypoglycemia who requires glucoseinfusion of >10–15 mg/kg/minto maintain normal serum glucose concentration. When blood glucoseconcentration is <40 mg/dL, inappropriate increasein serum insulin (>10 μU/mL) is considereddiagnostic.
  • Once presence of hyperinsulinemia hasbeen established through spontaneous or fasting-induced hypoglycemia,specific cause should be investigated by clinical, biochemical,and molecular genetic means.
  • Causes include genetic defects of beta-cellregulation and focal lesions (islet cell adenoma, focal islet cellhyperplasia).

    • Hormonal Deficiency

  • Causes ofhypoglycemia associated with endocrine deficiency include adrenalinsufficiency with or without growth hormone deficiency.
  • When hypoglycemia is discovered, bloodsample should be drawn for possible cortisol, growth hormone, thyroidhormone (thyroxine), thyroid-stimulating hormone, insulin, and adrenocorticotropichormone measurements. These tests should be performed if other clinicalsigns suggest hormonal deficiency or if no other cause can be foundfor hypoglycemia.

    • Ketotic Hypoglycemia

  • Hypoglycemiaassociated with ketonuria may occur in children 18 mos–5yrs of age as response to prolonged fast.
  • At time of hypoglycemia, serum insulinconcentration is appropriately low (≥5–10 μU/mL),which excludes hyperinsulinism.
  • Prolonged fast of 12–18 hrsusually reproduces hypoglycemia in susceptible individuals.

    • Drugs or Toxins

  • Insulinin excessive dosage may cause severe hypoglycemia. So may salicylateintoxication, which increases insulin secretion and may possiblyinterfere with gluconeogenesis.
  • Propranolol, a beta-adrenergic blockingagent, may cause hypoglycemia in children who have decreased oralintake from prolonged fasting or illness.
  • Because ethyl alcohol impairs gluconeogenesis,hypoglycemia may occur 6–8 hrs after acute alcohol ingestionor as early as 1 hr after ingestion in a young child, especiallyif the child has not been fed for several hours. In this circumstance,a blood alcohol level confirms diagnosis.

    • Hepatic Disease

    Hepatitis, cirrhosis, and Reye syndrome alsomay be associated with hypoglycemia. See Chap. 3, Alteration in Consciousness; Chap. 30, Hepatomegaly;and Chap. 36, Jaundice.

    Metabolic Disorders

    Glycogen Storage Diseases (Types O, I, III, VI)

  • Glycogenstorage disease type 0 is autosomal-recessive disorder caused bydeficiency in enzyme activity of hepatic glycogen synthetase.
  • Gene locus has been mapped to chromosome12p12.2.
  • Hypoglycemia and seizures occur withfasting. Serum insulin concentration is appropriately low.
  • Liver biopsy with enzyme assay confirmsdiagnosis.
  • Hypoglycemia and hepatomegaly may occurwith glycogen storage diseases types I, III, and VI (see Chap. 30, Hepatomegaly).

    • Disorders of Gluconeogenesis

    Fructose 1,6-Diphosphatase Deficiency

  • Resultsin hypoglycemia only during caloric restriction (e.g., with intercurrentillness or in fasting state).
  • Gene locus of this autosomal-recessivedisorder has been mapped to chromosome 9q22.2-q22.3.
  • Characteristic features include hepatomegaly,failure to thrive, ketonuria, and lactic acidosis.
  • Liver biopsy with enzyme assay is diagnostic.

    • Phosphoenolpyruvate Carboxykinase Deficiency

  • Severe fastinghypoglycemia, which may occur during first day of life, can occurwith this enzyme deficiency.
  • Diagnosis is made by enzyme assay fromliver biopsy.

    • Other

    Galactosemia, hereditary fructose intolerance,maple syrup urine disease, tyrosinemia, propionic acidemia, methylmalonicacidemia, and fatty acid oxidation disorders (especially medium-chainacyl-CoA dehydrogenase deficiency) are discussed in Chap. 3, Alteration in Consciousness,and Chap. 36, Jaundice.

    Systemic Disorders

    Septicemia, malnutrition, malabsorption,burns, and shock also may be associated with hypoglycemia.

    Hypocalcemia

  • May be definedas total serum calcium concentration of <7 mg/dLin preterm infants and <8 mg/dL in infants andchildren. Ionized calcium concentration of <3 mg/dLis also abnormal.
  • Clinical features include poor feeding,tremulousness, lethargy, vomiting, cramps, abdominal distension,seizures, apnea, and tetany (in non-neonates).
  • Suspicion of hypocalcemia should beconfirmed with measurement of total and ionized serum calcium. Agentsthat complex calcium in blood (e.g., citrate and long-chain freefatty acids) can reduce serum ionized calcium without a decreasein serum calcium.
  • In neonatal period, hypocalcemia mayoccur during first 1–2 days of life (early) or toward endof first week of life (late). Early form can occur in very-low-birth-weightinfants, infants with perinatal asphyxia, and infants of diabeticmothers. Hypoparathyroidism and maternal hyperparathyroidism areother causes of early hypocalcemia.
  • Late occurrence of hypocalcemia maybe due to intake of high-phosphate milk, decreased calcium intestinalabsorption, hypoparathyroidism, and hypomagnesemia. Failure of hypocalcemiato respond to intravenous calcium should suggest coexisting hypomagnesemia.
  • Principal causes of hypocalcemia ininfants and children include decreased intake (nutritional), diminishedintestinal absorption of calcium, excessive calcium excretion (hypercalciuria),chronic renal failure, drugs (furosemide), excessive use of sodiumphosphate enemas, hypoparathyroidism, and vitamin D deficiency.The latter 2 disorders are discussed in the next section.

    • Hypoparathyroidism

  • Causes includefamilial hypoparathyroidism, DiGeorge syndrome, postsurgical hypoparathyroidism,autoimmune disease, resistance to parathyroid hormone, and idiopathic.
  • Diagnosis is confirmed by low serumcalcium, high serum phosphorous, and low serum parathyroid hormoneconcentrations. Specific cause needs to be investigated.

    • Vitamin D Deficiency

  • Deficiencyof vitamin D intake or defect in its metabolism may lead to hypocalcemia. Resultof these disturbances is rickets, which involves failure of bonemineralization. Most infantile rickets occurs in exclusively breast-fedterm babies who are not exposed to the sun.
  • Other causes of rickets include

  • Vitamin Dmalabsorption
  • Defective vitamin D synthesis (acquired25-hydroxylase deficiency from liver disease)
  • Congenital l-alpha-hydroxylase deficiency(also called vitamin D–dependent rickets)
  • Acquired l-alpha-hydroxylase deficiency(chronic renal failure)
  • Altered vitamin D metabolism from anticonvulsanttherapy (phenobarbital, phenytoin)
  • Hypophosphatemia (familial vitaminD–resistant rickets)
  • Dietary phosphate deficiency
  • Multiple renal tubular defects (Fanconisyndrome)
  • Clinical manifestations of ricketsdepend on age of child and degree of mineral depletion. Mild involvementmay only cause biochemical changes, whereas more severe involvementusually produces some of the following physical findings: frontalbossing, craniotabes, delayed closure of the fontanelles and sutures,enlarged costochondral junctions, enlarged wrists and ankles, bilateralbowing of the legs, lumbar lordosis, and diminished growth.
  • Radiographic changes include cuppingand fraying of metaphyses of rapidly growing bone, decreased densityof shafts of long bones, and pathologic fractures.
  • Lab findings in rickets include normalor low serum calcium, low serum phosphorus (except with renal osteodystrophy),and high serum alkaline phosphatase.
  • Specific cause must be investigated.

    • Hypomagnesemia

  • Occurs whenserum magnesium concentration is <1.5 mg/dL.
  • Clinical signs include tremors, nystagmus,seizures, and muscle weakness (chronic).
  • Causes of neonatal magnesium deficiencyinclude

  • Decreasedmagnesium intake (maternal magnesium deficiency, small-for-gestational ageinfants)
  • Diminished intestinal absorption (extensivesmall intestine resection)
  • Increased magnesium losses (chronicdiarrhea, extrahepatic biliary atresia, neonatal hepatitis, decreasedrenal tubular reabsorption)
  • Drugs (aminoglycosides, diuretics)
  • Maternal hyperparathyroidism
  • Increased phosphate intake
  • In infants and children, causes include

  • Chronic diarrhea
  • Intestinal malabsorption
  • Chronic renal disease, drugs (aminoglycosides,diuretics, cisplatin, cyclosporine)
  • Diabetes mellitus

    • Hyponatremia

  • Definedas serum sodium concentration of <130 mEq/L.
  • In low-birth-weight infants, diureticsgiven for chronic lung disease is common cause.
  • Other causes in neonates include excessivehypotonic replacement of fluid losses, hypovolemia with loss ofsodium in excess of water, and inappropriate secretion of antidiuretichormone. The latter may occur with hypoxic-ischemic encephalopathy,intracranial hemorrhage, and bacterial meningitis.
  • Frequent cause in young infants isfeeding of large amounts of water without any electrolyte. Anothercause is persistent diarrhea with loss of sodium in excess of water.

    • Hypernatremia

  • Definedas serum sodium >150 mEq/L.
  • In low-birth-weight infants, hypernatremiais usually due to severe insensible water loss or treatment of metabolicacidosis with large amounts of sodium bicarbonate.
  • Main causes in infancy and childhoodinclude diarrhea with water losses out of proportion to sodium losses,extensive burns, diabetes insipidus, and chronic renal disease.

    • Uremia

    Various factors may cause seizures in childrenwith uremia, including uremia itself, hypocalcemia, hyponatremia,and hypertension.

    Bilirubin Encephalopathy (Kernicterus)

    Infants with kernicterus often have high-pitchedcry, poor feeding, decreased movements, opisthotonus, and seizures.Survivors usually have deafness, choreoathetosis, spasticity, andpsychomotor retardation (see Chap.3, Alteration in Consciousness).

    Pyridoxine Dependency

  • Pyridoxine(vitamin B6) dependency, a rare cause ofintractable neonatal seizures, usually presents in neonatal period,often during first day of life. Biochemical defect is unknown.
  • Seizures can be of any type. If noimmediate cause of neonatal seizures can be found and if they failto respond to usual therapy, trial of intravenous pyridoxine maybe given.
  • Cessation of seizures under EEG monitoringis best way to confirm diagnosis.

    • Inborn Errors of Metabolism

    These disorders include galactosemia, hereditaryfructose intolerance, glycogen storage diseases, disorders of gluconeogenesis,and organic acidemias (maple syrup urine disease, disorders of fattyacid oxidation). They are mentioned in the section Hypoglycemia and discussedin Chap. 3, Alteration in Consciousness,and Chap. 13, Developmental Delay.

    Selected Epileptic Syndromes

    In addition to conditions discussed below,childhood absence epilepsy causes seizures. There are also unknowncauses.

    Neonatal Seizures

  • Manifestationsof seizures in neonates may be different from those in infants andchildren. Neonatal seizures are often subtle and change from momentto moment. They rarely occur as isolated events but usually occurrepeatedly over a few hours or days. Generalized tonic-clonic seizuresrarely if ever occur in neonates. Main seizure types in neonatesare subtle (associated motor automatisms), clonic (focal or multifocal),tonic (focal or generalized), and myoclonic (focal, multifocal,generalized).

  • Mostcommon type of neonatal seizure is subtle, which may involve eyechanges (conjugate eye deviation, eye fluttering, blinking), mouthmovements (chewing, sucking, drooling, tongue thrusting), autonomicchanges (tachycardia, BP changes, pupillary dilatation), or apnea.Usually unassociated with ictal EEG changes, except when tonic eyedeviation occurs.
  • Clonic seizures involve rhythmic jerkingof 1 part of body that may be focal or multifocal. Focal seizurein neonates does not necessarily signify focal brain pathology.Can occur with generalized metabolic disturbance (e.g., hypoglycemia).Ictal EEG usually shows rhythmic discharges.
  • Tonic seizures involve extension oflimbs and are usually generalized. Seen most commonly with severebrain injury (hypoxic-ischemic encephalopathy, intracranial hemorrhage)and is usually not accompanied by ictal EEG changes.
  • Myoclonic seizures are characterizedby rapid isolated jerks of entire body or body parts. Usually signifiessevere brain injury (e.g., hypoxic-ischemic encephalopathy). Mayevolve into infantile spasms. Generalized myoclonic seizures areusually associated with abnormal ictal EEG, whereas it is unusualto see ictal changes with focal or multifocal myoclonic seizures.

    • Benign Neonatal Epilepsy

  • Benign formof neonatal seizures has been described in some families. Genetictransmission is autosomal-dominant and 2 genetic loci have beenmapped.
  • Seizures are often mixed, with tonicand clonic movements and motor automatisms.
  • Neurologic exam is normal.
  • Spontaneous remission usually occursafter several months.

    • Infantile Spasms (West Syndrome)

  • Infantilespasms, a form of generalized epilepsy, usually begin at 4–8mos of age.
  • The flexor spasm (salaam or jackknifeattacks) with sudden flexion of head, neck, and trunk, lasts a fewseconds and tends to occur in repetitive series of attacks, whichmay number up to several hundred episodes in 1 day.
  • Usual EEG finding is hypsarrhythmiapattern, which consists of high-voltage, irregular slow waves withspike-and-wave complexes.
  • Hypoxic-ischemic encephalopathy, perinatalinfections, cerebral dysgenesis, and various genetic (tuberous sclerosis)and metabolic disorders (phenylketonuria) are common causes of thistype of epilepsy.

    • Lennox-Gastaut Syndrome

  • Characterizedby seizures, developmental delay, and characteristic EEG pattern.It is not a pathologic entity, but rather diffuse encephalopathywith many causes (e.g., perinatal asphyxia, cerebral malformation,head trauma, CNS infection, metabolic disorders, and neurodegenerativediseases).
  • Seizures usually begin in children <3yrs of age and are difficult to control.
  • More than 1 seizure type may occur,and most common types are tonic-clonic, tonic, and myoclonic.
  • EEG usually shows bilateral, generalized,synchronous sharp and slow-wave discharges.

    • Benign Focal Epilepsy with Centrotemporal Spikes

  • Most commonsyndrome of simple partial epilepsy in childhood. Onset is usually2–14 yrs of age, with peak at 9–10 yrs.
  • Seizures are primarily motor and predominantlyaffect face and oropharyngeal musculature, often lasting 30–60secs and occurring usually while asleep or upon awakening.
  • Neurologic exam is normal. TypicalEEG shows repetitive spike focus in centrotemporal area.
  • Recurrences after 16 yrs of age areunusual.

    • Temporal Lobe Epilepsy

  • Temporallobe seizures are most common cause of partial complex seizuresin adolescents.
  • Usually preceded by aura, which mayconsist of head deviation and posturing in children <2 yrsof age, epigastric sensation associated with fear in young children,and hallucinations in older children.
  • Onset is often noted by staring episodes,lip smacking, or chewing movements.
  • Duration is usually 1–2 mins,which is longer than with absence seizures. Period of confusionor tiredness usually follows.
  • MRI may reveal anatomic abnormality(e.g., hamartoma, slow-growing glioma, cyst, arteriovenous malformation,or mesial temporal sclerosis).

    • Juvenile Myoclonic Epilepsy

  • Usual onsetis 12–18 yrs of age.
  • Myoclonic jerks affect mainly shouldersand arms and rarely lower extremities.
  • Consciousness is usually preserved.
  • Tonic-clonic or absence seizures alsomay occur.
  • Sleep deprivation and photic stimulationcan trigger this type of seizure.
  • Characteristic EEG shows generalizedspike/polyspike-and-wake discharges.

    • Posttraumatic Epilepsy

  • Head traumacan cause seizures at any age.
  • Risk of seizures is related to severityof trauma. Children with cerebral contusion, intracerebral hematoma,or loss of consciousness for >24 hrs are at risk for developingseizures.
  • Generalized or focal seizures can occuras acute reaction of the brain to trauma, in 1–2 wks followingtrauma, or months later.

    • Diagnostic Approach

    Neonatal Seizures

    Phenomena That May Be Confused with Seizures

    Determining whether a seizure has occurredmay be difficult in some neonates. Seizures may consist of clonicmovements, tonic posturing of extremity, repetitive random or suckingmovements, or eye deviation. Recurrent apnea also may occur as amanifestation of a seizure disorder, but it is rarely the only manifestation.Jitteriness and benign myoclonic phenomena must be distinguishedfrom seizures.

    Jitteriness

    Jitteriness is stimulus sensitive and hasa tremulous quality. It ceases when extremity is held.

    Benign Neonatal Sleep Myoclonus

  • Occurs duringdrowsiness and sleep but not during wakefulness.
  • Consists of isolated jerking movementsof arm or leg.
  • Pathologic myoclonic jerks in newbornsare not related to sleep; face and trunk may be involved, and EEGis abnormal.

    • Evaluation

  • Historyand physical exam suggest most likely causes of neonatal seizures.
  • Certain tests should be performed initially:CBC with differential; blood glucose and urea nitrogen; and serumelectrolytes, creatinine, calcium, phosphorus, and magnesium.
  • If meningitis or septicemia is suspected,spinal fluid analysis with appropriate cultures, blood culture,UA, and urine culture should be performed.
  • Imaging of brain with head U/Splus CT or MRI is useful for suspected brain malformations and intracranialhemorrhage.
  • The following tests should be consideredfor suspected metabolic disorders: serum ammonia, lactate, pyruvate,carnitine, liver function tests, amino acids, blood pH, and PCO2;urine for reducing sugars, ketones, and organic acid analysis; andcerebrospinal fluid glycine. Simultaneous video-EEG recording mayclarify whether seizures are occurring and if so, what type theyare.
  • Blood glucose determination confirmspresence of hypoglycemia.

  • With symptomatic hypoglycemia, intravenousglucose should be given, but before glucose is given, blood sampleshould be drawn and held for subsequent tests.
  • Serum insulin level of >10μU/mL in presence of hypoglycemia is evidence forhyperinsulinemia.
  • Serum cortisol level of <10μg/dL suggests adrenal insufficiency. Low serum cortisoland growth hormone levels suggest pituitary disease.
  • Presence of hepatomegaly suggests galactosemia,hereditary fructose intolerance, or glycogen storage disease (typesI, III, VI). Urine positive for reducing sugars occurs with galactosemiaand hereditary fructose intolerance.
  • If diagnosis is uncertain and seizuresdo not respond to therapy, 100–200 mg of intravenous pyridoxinemay be given, while monitoring clinical and EEG responses.

    • Postneonatal Seizures

    Phenomena That May Be Confused with Seizures

    Clinical phenomena that may be confused withseizures are syncope, breath-holding spells, tics, benign paroxysmalvertigo, pseudoseizures, night terrors, migraine, and spasmus nutans.Manifestations of each are briefly described and contrasted withthose of seizures.

    Syncope

  • May be precededby dizziness or nausea. There is loss of postural tone, and individual collapses.Bradycardia and lowered BP occur in neurocardiogenic syncope (commonfaint).
  • History may include evidence of anxiety,hyperventilation, systemic illness, fasting, or prolonged standing,especially in warm weather or in closed quarters.
  • Tonic-clonic movements are uncommon,and urine incontinence is rare.
  • After episode, confusion is uncommonand amnesia does not occur.

    • Breath-Holding Spells

  • Unusualbefore 6 mos of age and usually cease by 6 yrs of age.
  • Pallid breath holding, which is consideredvariant of neurocardiogenic syncope, usually follows acute painor an injury. Infant or child becomes pale and loses consciousness;however, complete recovery occurs in 1–2 mins.
  • More common is cyanotic breath-holdingspell, where infant or child cries, holds breath during expiration,and turns dusky until breathing occurs again. Prolonged episodemay result in tonic-clonic movements and loss of consciousness.

    • Tics

    Recurrent involuntary movements that maymimic seizures. No loss or change in consciousness or postictalphenomena occur. Verbal tics also occur, especially in Tourettesyndrome.

    Benign Paroxysmal Vertigo

  • Usuallydevelops in children 2–6 yrs of age.
  • Sudden episodes are associated withfalling, refusing to walk, nausea, vomiting, and nystagmus. Duringthe episode, ability to communicate and talk is retained.
  • Episodes may last seconds to minutesand can occur daily or every few months.

    • Pseudoseizures (Nonepileptic Events)

  • Typicallyoccur at 10–18 yrs of age and are more common in girls.They may be seen, however, in children as young as 4–6yrs of age.
  • These events represent a form of conversionreaction, sometimes as a result of physical or sexual abuse.
  • Episodes can mimic generalized tonic-clonic,tonic, and complex partial seizures, but they differ from true seizuresin several ways. Onset of movements gradually builds up to paroxysmcompared with sudden onset of epileptic attack. Motor movementsare not true clonic movements but range from quivering to flailingof extremities. Postures and verbalizations are unusual.
  • Afterward, most individuals becomeimmediately responsive and do not experience postictal state.
  • Urination and tongue biting are infrequentbut may occur. Episodes never occur during sleep and only infrequentlywhen child is alone.
  • Ictal EEG shows no paroxysmal discharges.
  • Pseudoseizures also can occur in individualswho have true seizures.

    • Night Terrors

    Common in children 5–7 yrs of age,particularly in boys, and occur during slow-wave sleep. Childrenscream, thrash around, and appear frightened. Seem unaware of theirparents and surroundings. Difficult to console and do not rememberepisode. In contrast, nightmares occur during rapid eye movement sleep,and children can often recall episode.

    Migraine

  • Transientconfusional states and focal neurologic signs may occur during migraine episode.
  • Family history of migraine usuallyexists.
  • Migraine and seizures may occur insame individual, so careful evaluation is important.

    • Spasmus Nutans

    Characterized by triad of head nodding, nystagmus,and torticollis.

    Evaluation

  • Once ithas been established that a seizure has occurred, seizure type andcause must be determined if possible. Direct observation or carefulhistory may permit physician to determine seizure type, but thisis not always possible, and EEG is often helpful.
  • Age of onset, type of seizure, medicalhistory, circumstances in which seizure occurs, and physical examhelp determine whether patient has epileptic syndrome. Importantto recognize particular epileptic syndrome to determine appropriatetherapy and prognosis as well as to assess genetic risk.
  • Child who presents with fever and seizureusually has either febrile seizure or intracranial infection (meningitisor encephalitis).
  • Lumbar puncture should be performedin any child with suspected meningitis or encephalitis.
  • Because clinical exam is more reliablein child >18 mos of age than in younger infant, lumbarpuncture may not be necessary in older child with simple febrileseizure who appears otherwise well and has normal physical exam.
  • With occurrence of nonfebrile seizure,serum sodium, glucose, calcium, magnesium, creatinine, and bloodurea nitrogen should be measured. Approach to hypoglycemia has alreadybeen discussed. EEG should be performed except for child with typicalfebrile seizure.
  • History of head trauma suggests presenceof contusion, skull fracture, or intracranial hemorrhage. Childabuse is frequent cause of head trauma, and other clues (e.g., obviousbruising) may be seen. Shaking injury may produce extensive traumawith no visible evidence of injury.
  • With history of head trauma and seizure,CT should be performed.
  • With evidence of increased intracranialpressure or focal findings including focal seizures, intracranialmass lesion should be suspected and CT or MRI should be performed.MRI is preferred over CT for diagnosis of small hamartomas or othermalformations, neuronal migrational disorders, and mesial temporalsclerosis.
  • Drug or poison ingestion is anotherpossible cause of acute seizure, and history may be diagnostic.Otherwise, urine toxicology screen may confirm diagnosis.
  • Cerebral angiography is useful in thediagnosis of a vascular lesion (e.g., cerebral aneurysm or arteriovenousmalformation).
  • Other tests should be ordered, dependingon presence of other findings (e.g., progressive neurologic syndrome).
  • If uncertain whether seizures are occurring,simultaneous video-EEG recording can be performed. Although EEGis useful to help confirm diagnosis of epilepsy and classify typeof seizures, normal interictal EEG may occur with epilepsy and abnormalEEG does not confirm diagnosis unless seizure has been clinicallyrecognized. EEG should be recorded during wakefulness and sleep,and maneuvers that may activate seizure activity (e.g., hyperventilation,photic stimulation, and sleep deprivation) should be performed.
    • >>>>>>>>>>>>>

    » READ BOOK EXCERPT ONLINE »

    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    Aura: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Obtain a thorough history of the patient's headache or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    Then perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Carpopedal spasm: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient isn't in distress, obtain a detailed history. Ask about the onset and duration of the spasms and ask for a description of pain they produce. Also ask about related signs and symptoms of hypocalcemia, such as numbness and tingling of the fingertips and feet, other muscle cramps or spasms, and nausea, vomiting, and abdominal pain. Check for previous neck surgery, calcium or magnesium deficiency, tetanus exposure, and hypoparathyroidism.

    During the history, form a general impression of the patient's mental status and behavior. If possible, ask family members or friends if they've noticed changes in the patient's behavior. Mental confusion or even personality changes may occur with hypocalcemia.

    Inspect the patient's skin and fingernails, noting dryness or scaling and ridged, brittle nails.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Level of consciousness, decreased: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Try to obtain history information from the patient, if he's alert, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient's behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

    Because a decreased LOC can result from a disorder affecting any body system, tailor the remainder of your evaluation according to the patient's associated symptoms.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Myoclonus: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient is stable, evaluate his level of consciousness (LOC) and mental status. Ask about the frequency, severity, location, and circumstances of myoclonus. Has he ever had a seizure? If so, did myoclonus precede it? Is myoclonus ever precipitated by a sensory stimulus? During the physical examination, check for muscle rigidity and wasting, and test deep tendon reflexes. Then perform a neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Paralysis: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient is in no immediate danger, perform a complete neurologic assessment. Start with the history, relying on family members for information if necessary. Ask about the onset, duration, intensity, and progression of paralysis and about the events preceding its development. Focus medical history questions on the incidence of degenerative neurologic or neuromuscular disease, recent infectious illness, sexually transmitted disease, cancer, or recent injury. Explore related signs and symptoms, noting fevers, headaches, vision distur-bances, dysphagia, nausea and vomiting, bowel or bladder dysfunction, muscle pain or weakness, and fatigue.

    Next, perform a complete neurologic examination, testing cranial nerve (CN), motor, and sensory function and deep tendon reflexes (DTRs). Assess strength in all major muscle groups, and note muscle atrophy. (See Testing muscle strength, pages 410 and 411.) Document all findings to serve as a baseline.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Seizures, complex partial: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don't approach him if he's angry or violent.) Calmly encourage him to sit down, and remain with him until he's fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings. Obtain a history. Has the patient experienced a seizure in the past? Has he had a recent head injury? Has he experienced any fever, headaches, or periods of confusion? Obtain a complete drug history. Take his vital signs and perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Seizures, generalized tonic-clonic: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If you didn't witness the patient's seizure, obtain a description from his companion. Ask when the seizure started and how long it lasted. Did the patient report unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body right away? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have other seizures before recovering?

    If the patient may have sustained a head injury, observe him closely for loss of consciousness, unequal or nonreactive pupils, and focal neurologic signs. Does he complain of headache and muscle soreness? Is he increasingly difficult to arouse when you check on him at 20-minute intervals? Examine his arms, legs, and face (including tongue) for injury, residual paralysis, or limb weakness.

    Next, obtain a history. Has the patient ever had generalized or focal seizures before? If so, do they occur frequently? Do other family members also have them? Is the patient receiving drug therapy? Is he compliant? Also, ask about sleep deprivation and emotional or physical stress at the time the seizure occurred.

    Next, assess the patient's level of consciousness (LOC) and proceed with a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Seizures, simple partial: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Be sure to record the patient's seizure activity in detail; your data may be critical in locating the lesion in the brain. Does the patient turn his head and eyes? If so, to what side? Where does movement first start? Does it spread? Because a partial seizure may become generalized, you'll need to watch closely for loss of consciousness, bilateral tonicity and clonicity, cyanosis, tongue biting, and urinary incontinence. (See “Seizures, generalized tonic-clonic,” page 552.)

    After the seizure, ask the patient to describe exactly what he remembers, if anything, about the seizure. Check the patient's LOC, and test for residual deficits (such as weakness in the involved extremity) and sensory disturbances.

    Then obtain a history. Ask the patient what happened before the seizure. Can he describe an aura or did he recognize its onset? If so, how—by a smell, a vision disturbance, or a sound or visceral phenomenon such as an unusual sensation in his stomach? How does this seizure compare with others he has had?

    Also, explore fully any history—recent or remote—of head trauma. Check for a history of stroke or recent infection, especially with fever, headache, or stiff neck.

    Perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Seizures, absence: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If you suspect a patient is having an absence seizure, evaluate its occurrence and duration by reciting a series of numbers and then asking him to repeat them after the attack ends. If the patient has had an absence seizure, he can't do this. Alternatively, if the seizures are occurring within minutes of each other, ask the patient to count for about 5 minutes. He'll stop counting during a seizure and resume when it's over. Look for accompanying automatisms. Find out if the family has noticed a change in behavior or deteriorating schoolwork.

    Next, perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    TREMOR AND OTHER INVOLUNTARY MOVEMENTS: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The workup of tremor and other involuntary movements involves most of all a good history. A family history may identify familial tremor. Look for exposure to lead, manganese, and various drugs. The neurologic examination is important as it will determine the type of tremor. Rapid fine tremors (8–20/s) are suggestive of hyperthyroidism and emotional disorders. Coarser tremors at rest suggest Parkinsonism, whereas a flapping tremor of 4 to 8 per second suggests Wilson disease. The association of other neurologic signs helps to pin down the diagnosis. Spasms of pain suggest a thalamic syndrome, ataxia suggests Friedreich ataxia, and loss of memory suggests manganese toxicity. Laboratory tests will be useful in selected cases. Blood lead, manganese, copper, and ceruloplasmin levels may be necessary. A triiodothyronine (T3), thyroxine (T4), and free T4 index will confirm the diagnosis of Graves disease. Other tests that may be helpful may be found in Appendix A or listed below.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    FACIAL PARALYSIS: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The clinical picture will frequently help to determine the cause of facial paralysis. Peripheral facial palsy as occurs in Bell palsy involves the forehead muscles and there is difficulty in closing the eyelid, whereas central facial palsy involves the face and lips and there is often associated hemiplegia or monoplegia. When there is exclusively a peripheral facial palsy without hearing loss or other neurologic signs, Bell palsy should be strongly suspected, although diabetes and myasthenia gravis need to be excluded. A bilateral peripheral nerve palsy should make one consider Guillain–Barré syndrome; be on the lookout for paralysis of the extremities as well. Bilateral facial palsy is also seen in myotonic dystrophy and myasthenia gravis. A “Bell palsy” with hearing loss and an aural discharge should prompt consideration of mastoiditis and petrositis. If there is hearing loss without a discharge, the possibility of an acoustic neuroma or cholesteatoma must be entertained. The association of a central facial palsy with hemiplegia brings up a host of possibilities including subdural hematoma, brain abscess, brain tumor, and cerebrovascular accident. The workup of these conditions is considered on page 222. If the patient has clinical Bell palsy, one could start a therapy without a workup, but it is wise to get an x-ray of the skull and mastoids to rule out mastoiditis and petrositis and a glucose tolerance test to rule out diabetes. An acetylcholine receptor antibody titer or Tensilon test would only be ordered if the palsy were intermittent or there were other cranial nerve signs. If a middle ear infection or acoustic neuroma is suspected, the patient needs x-ray of the mastoids and petrous bones and a CT scan or MRI of the brain and auditory canal.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    WEAKNESS OR PARALYSIS OF ONE OR MORE EXTREMITIES: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The site of weakness is determined by associated symptoms and signs. Fasciculations suggest nerve root or anterior horn cell involvement, whereas sensory changes suggest peripheral nerve or spinal cord involvement. A combination of spasticity in the lower extremities and flaccid and atrophic weakness in the upper extremities suggests cervical cord involvement. Cranial nerve lesions in association with paraplegia or quadriplegia usually indicate a brainstem lesion. The workup will depend on the site in which the pathology is suspected to be located. If muscle is the site, then an EMG or biopsy is indicated. If the myoneural junction is involved, a Tensilon test is done. Peripheral nerve lesions require a more extensive workup, including a glucose tolerance test, blood lead level, urine for porphobilinogens, EMG, nerve conduction velocity (NCV) test, and possibly a muscle biopsy. Spinal cord lesions may require x-ray of the spine, CT scan or MRI, myelography, discography, and spinal fluid analysis. Brainstem and cerebral lesions are best screened with a skull x-ray, MRI, or CT scan before a spinal tap or arteriogram is considered.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    LYMPHADENOPATHY, GENERALIZED: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Obviously, it is tempting simply to do a lymph node biopsy, but certain other procedures should be done first. If the patient is febrile, febrile agglutinins, monospot test, blood cultures, and cultures of any other suspicious body fluid should be made. A fluorescent treponemal antibody absorption test (FTA-ABS) test should be done as well as a chest x-ray and tuberculin test to rule out tuberculosis. A blood count usually shows leukemia, but a bone marrow biopsy may be necessary to diagnose leukemia, Hodgkin lymphoma, and the reticuloendothelioses. Other x-rays, skin tests, and special diagnostic procedures may be necessary.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    WEAKNESS AND FATIGUE, GENERALIZED: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The association of other symptoms and signs with generalized weakness and fatigue is very important in pinning down a diagnosis. Generalized lymphadenopathy and fatigue suggest infectious mononucleosis, lymphoma, or tuberculosis or other chronic infection such as acquired immunodeficiency syndrome (AIDS). Weakness, weight loss, and polyphagia with polyuria and polydipsia would suggest hyperthyroidism or diabetes mellitus. Generalized weakness with polyuria and no significant weight loss suggests hyperparathyroidism. Weakness with pallor suggests some type of anemia. Weakness and weight loss without polyuria or polyphagia suggest malignancy or malabsorption syndrome. Weakness with other significant neurologic signs and symptoms prompts the consideration of muscular dystrophy, amyotrophic lateral sclerosis, or multiple sclerosis. Weakness with drug or alcohol use prompts the investigation of drug or alcohol abuse. Caffeine, especially in large quantities, can also cause significant weakness and chronic fatigue. The initial workup of weakness and fatigue requires a CBC, sedimentation rate, drug screen, chemistry panel, thyroid profile, ANA, chest x-ray, and echocardiogram (ECG). If muscular dystrophy or dermatomyositis is suspected, urine tests for creatinine, creatine, and myoglobin can be done. Ultimately, a muscle biopsy may be indicated. If myasthenia gravis is suspected, serum for acetylcholine receptor antibody may be done. If Addison disease is suspected, a serum cortisol test may be done. A 24-hour urine aldosterone level may be done to exclude primary aldosteronism. Serum parathyroid hormone (PTH) may be done to exclude hyperparathyroidism. It would be wise to consult an infectious disease specialist before ordering an expensive workup. It would also be wise to consult an oncologist when searching for a malignancy before ordering an expensive workup. When all tests have negative findings, many clinicians have been tempted to make a diagnosis of chronic fatigue syndrome. It is questionable whether this is truly a disease or not.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    Seizures - Case 19-3: 8-Month-Old Boy: I. History of Present Illness
    (Pediatric Complaints and Diagnostic Dilemmas)

    An 8-month-old boy was well until 1 week before admission, when he was found by his mother having a “seizure.” He had shaking and jerking of all extremities that did not stop when his extremities were held. He did not respond to touch or stimulation. There was no cyanosis. The episode lasted approximately 15 minutes. By the time Emergency Medical Services personnel arrived, the patient was alert and feeding on a bottle. He was not taken to the hospital. His last feeding had been approximately 3 hours before the event. Two days later, he was evaluated by his primary physician, who performed the following laboratory evaluations: glucose (during feeding), 121 mg/dL; alanine aminotransferase (ALT), 73 U/L; aspartate aminotransferase (AST), 93 U/L; γ-glutamyl transferase (GGT), 28 U/L; and cholesterol, 423 mg/dL. These laboratory studies were repeated 2 days later, with similar results except the glucose was 16 mg/dL. Head CT and EEG were normal. He was hospitalized for additional evaluation.

    II. Past Medical History

    The patient was born at 38 weeks' gestation with a birth weight of 3,400 g. His delivery was complicated by meconium aspiration. He was treated with supplemental oxygen and empiric antibiotics for 3 days. He also had hypoglycemia requiring intravenous dextrose and bottle feedings every 1.5 hours. This resolved, and he was discharged home on the fourth day of life. At 3 months of life, he had been diagnosed with otitis media and received oral antibiotics. There was no family history of seizures or mental retardation.

    III. Physical Examination

    T, 36.2°C; RR, 20/min; HR, 90 to 110 bpm; BP, 120/55 mm Hg; SpO2, 100% in room air
    Height, 25th percentile; weight, 10th percentile; head circumference, 25th percentile
    On examination, he was thin but playful and interactive. The anterior fontanel was open and flat. His pupils were symmetrically reactive to light. The heart sounds were normal, and the lungs were clear to auscultation. His abdomen was slightly protuberant, with a liver edge that was firm and palpable 6 cm below the right costal margin. The spleen tip was just palpable below the left costal margin. There was no ascites or palpable abdominal mass. The infant was circumcised and had normal male genitalia. The neurological examination was normal. He was able to sit without support and maintained good head control. Deep tendon reflexes were 2+ and symmetric. The gag reflex was intact. There were no hyperpigmented or hypopigmented skin lesions.

    IV. Diagnostic Studies

    Serum chemistry values included sodium, 137 mmol/L; potassium, 5.5 mmol/L; chloride, 100 mmol/L; bicarbonate, 13 mmol/L; calcium, 10.5 mg/dL; phosphorous, 6.5 mg/dL; and serum glucose 20 mg/dL. The cholesterol and triglyceride concentrations were 465 and 4,070 mg/dL, respectively. Hepatic function tests included AST, 125 U/L; ALT, 155 U/L; GGT, 564 U/L; total bilirubin, 0.6 mg/dL; and albumin, 4.0 g/dL. Serum and urinary ketones were present. The WBC count, hemoglobin, and platelet count, as well as prothrombin and partial thromboplastin times, were normal. Blood, urine, and stool cultures were obtained.

    » READ BOOK EXCERPT ONLINE »

    Source: Pediatric Complaints and Diagnostic Dilemmas, 2003


     » Next page: Signs of Grand mal seizures

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