Diseases » Paraplegia » Diagnosis

Diagnosis of Paraplegia

Paraplegia Diagnosis: Book Excerpts

• Ask the Following Questions - FACIAL PARALYSIS
• Ask the following questions - EXTREMITY PAIN, LOWER EXTREMITY
• Ask the Following Questions - PARESTHESIAS OF THE LOWER EXTREMITY
• Differential Diagnosis - Paraplegia
• Differential Diagnosis - Facial Paralysis & Bell's Palsy
• Differential Diagnosis - Facial Paralysis
• Approach to the Diagnosis - FACIAL PARALYSIS
• Approach to the Diagnosis - WEAKNESS OR PARALYSIS OF ONE OR MORE EXTREMITIES
• Approach to the Diagnosis - EXTREMITY MASS
• History and physical examination - Analgesia
• History and physical examination - Paralysis
• Diagnosis - Vocal cord paralysis
• History and physical examination - Analgesia
• History and physical examination - Paralysis
• Diagnosis - Vocal cord paralysis
• History - Analgesia
• History - Paralysis
• History - Paralysis
• History and physical examination - Analgesia
• History and physical examination - Paralysis
• Approach to the Diagnosis - FACIAL PARALYSIS
• Approach to the Diagnosis - WEAKNESS OR PARALYSIS OF ONE OR MORE EXTREMITIES
• Approach to the Diagnosis - EXTREMITY MASS

Diagnostic Tests for Paraplegia: Online Medical Books

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

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.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

EXTREMITY PAIN, LOWER EXTREMITY: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is the extremity pain of acute or gradual onset? Acute onset would suggest arterial embolism, deep vein thrombophlebitis, and cellulitis. If there is a history of trauma, it would suggest a fracture, sprain, or torn ligament.
2. Is there limitation of motion of the joints? A positive Patrick's test would indicate hip pathology, including greater trochanter bursitis. A positive McMurray test would indicate a torn meniscus.
3. Are there positive neurologic findings? A positive femoral stretch test would suggest a herniated disk at L2-3 or L3-4, whereas a positive Lasègue's sign would indicate a herniated disk at L4-5 or L5 to S1. Combined motor and sensory deficits may indicate radiculopathy or neuropathy.
4. Is there a positive Homans' sign? This is a very important examination, as one would not want to miss a deep vein thrombophlebitis.
5. Is there diminished or absent peripheral pulses? Diminished or absent pulses would suggest arterial embolism, peripheral arteriosclerosis, or Leriche's syndrome (thrombosis of the terminal aorta).
6. Is there focal tenderness, swelling, or erythema of the extremity? This would suggest cellulitis, superficial thrombophlebitis, osteomyelitis, lymphangitis, and other types of infections. Tenderness without significant swelling or erythema would be suggestive of bursitis or deep vein thrombophlebitis.

DIAGNOSTIC WORKUP

Often bursitis and myofascitis can be diagnosed by the dramatic relief obtained from a lidocaine injection. If there is clear-cut joint pathology, an x-ray of the joints, arthritis profile, and synovial fluid analysis will usually provide a diagnosis. MRI is useful in the diagnosis of a torn meniscus. If a deep-pain thrombophlebitis is suspected, venous Doppler ultrasound, impedance plethysmography, or a contrast venogram may be done. If an arterial embolism or chronic peripheral arterial disease is suspected, femoral angiography can be done. If a herniated disk or other pathology of the lumbar spine is suspected, plain films of the lumbar spine should be obtained. It might be wise at this point also to obtain a CBC, sedimentation rate, and chemistry panel to determine the alkaline phosphatase, calcium, and phosphorus. In older males, tests for acid phosphatase and PSA should be done.

If these tests are unrevealing, it is wise to refer the patient to a neurologic specialist before any more expensive tests are ordered. He will probably order a CT scan of the lumbar spine and may do nerve conduction velocity studies, EMG examinations, or dermatomal SSEP studies as indicated. In difficult neurologic problems, a combined myelography and CT scan is preferred over MRI. Bone scans will help diagnose obscure fractures and osteomyelitis, both of the lumbar spine and the lower extremities.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

PARESTHESIAS OF THE LOWER EXTREMITY: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Are the pulses diminished? The presence of diminished pulses should suggest peripheral arteriosclerosis or Leriche's syndrome.
2. Is there associated pain in the involved extremity? The presence of pain in the involved extremity should suggest lumbar spondylosis, spinal stenosis, cauda equina tumor, spondylolisthesis, herniated disk, and pelvic tumors.
3. Is there a positive straight-leg raising test and/or decreased Achilles reflex? These findings suggest a herniated disk of L4-5 or L5 to S1, lumbar spondylosis, spinal stenosis, a cauda equina tumor, or spondylolisthesis.
4. Is there a positive femoral stretch test or decreased knee jerk? These findings suggest a herniated disk of L3-4 or L2-3 or lumbar spondylosis.
5. Are there diffuse hyperactive reflexes? These findings suggest multiple sclerosis, pernicious anemia, degenerative diseases of the spinal cord such as syringomyelia, spinal cord tumor, or other space-occupying lesions. It may also suggest anterior spinal artery occlusion.
6. Are there diffuse hypoactive reflexes? The presence of diffuse hypoactive reflexes would suggest poliomyelitis, Guillain-Barré syndrome, cauda equina tumor, metastatic tumor of the lumbar spine, and, occasionally, pernicious anemia or peroneal neuropathy. Also, peripheral neuropathy will present with diffuse hypoactive reflexes.
7. Is there incontinence associated with the hypoactive reflexes? The presence of incontinence with the hypoactive reflexes may indicate poliomyelitis, cauda equina tumor, or metastatic tumors to the lumbar spine.

DIAGNOSTIC WORKUP

The basic diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, arthritis panel, VDRL test, and x-ray of the lumbosacral spine. A serum B ₁₂ and folic acid should be done if pernicious anemia is suspected. If these tests are negative, an orthopedic or neurologic specialist should be consulted. A CT scan of the lumbosacral spine, a nerve conduction velocity study, and an EMG may all be necessary in the workup. MRI is more expensive and often unnecessary.

Combined myelography and CT scan is often useful in evaluating the need for surgery. A bone scan may be helpful in diagnosing occult fractures, metastases, or osteomyelitis.

If multiple sclerosis, Guillain-Barré syndrome, or central nervous system lues are suspected, a spinal tap may be done. SSEP studies are useful in diagnosing multiple sclerosis.

A neuropathy workup may be necessary. This involves a glucose tolerance test to rule out diabetes; urine tests for porphyrins and porphobilinogen to rule out porphyria; quantitative urine niacin, thiamine, pyridoxine, and other B vitamins after loading, an ANA and anti-dsDNA test to rule out collagen disease; serum protein electrophoresis and immunoelectrophoresis to diagnose various collagen diseases and macroglobulinemia; a lymph node biopsy and Kveim test for sarcoidosis; nerve conduction velocity studies and EMG to establish the presence of a neuropathy; thyroid profile to rule out hypothyroidism or hyperthyroidism; HIV antibody titers; blood levels for heavy metals such as lead to rule out lead or arsenic neuropathy; and skin and muscle biopsies to rule out various collagen diseases. A trial of therapy is often necessary to rule out the nutritional neuropathies.

Lumbar puncture, as already mentioned, is useful in diagnosing Guillain-Barré syndrome. Nerve biopsy may be necessary when all the above procedures are negative.

RBC transketolase activity is decreased in beriberi and the serum pyruvate and lactate levels are elevated.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

• Myelopathy
  –Compressive (e.g., spondylytic, spinal epidural abscess or hematoma)
  –Traumatic
  –Metabolic (e.g., vitamin B₁₂ deficiency)
  –Infectious (e.g., HIV or other viral myelitis, botulism)
  –Inflammatory (e.g., multiple sclerosis, SLE, vasculitis, transverse myelitis)
  –Vascular (spinal cord or cerebral infarct)
  –Neoplastic
• Congenital
  –Dysraphism: Spina bifida, tethered cord
  –Cerebral palsy
• Syringomyelia
• Cauda equina syndrome
  –Caused by compression of the cauda equina, often by a central disc herniation
  –Variable presentation with lower extremity weakness, sensory loss, pain, lower motor neuron findings on examination, and bowel/bladder disturbances
• Polyradiculopathy
• Peripheral neuropathy
  –Usually results in a chronic or insidious onset of lower extremity weakness (except Guillain-Barré syndrome, which may result in weakness over hours to days)
  –Guillain-Barré syndrome: Also results in upper extremity weakness
  –Myasthenia gravis
  –Eaton-Lambert syndrome
  –Amyotrophic lateral sclerosis
  • HTLV-I associated myelopathy
  • Hereditary spastic paraparesis
  • Spinocerebellar or Friedreich's ataxia
  • Myopathies (e.g., muscular dystrophy) may result in paraparesis, but usually also result in upper extremity weakness
  • Parafalcine meningioma
    –May result in bilateral lower extremity weakness by compressive effects on the medial frontal lobe bilaterally
  • Bilateral anterior cerebral artery infarction
  • Medications (e.g., pancuronium)
  • Periodic paralysis (secondary to hyper- or hypokalemia)
  • Tick paralysis
  • Lyme disease
  • Psychogenic (e.g., conversion disorder)

  Workup and Diagnosis

  • History and physical examination
    –Determine whether the weakness is more likely secondary to an upper or a lower motor neuron disorder (e.g., symmetric lower extremity weakness with hyperreflexia, positive Babinski's signs, and a dermatomal area of sensory loss suggests a myelopathy, whereas symmetric lower extremity weakness with areflexia and flexor plantar responses suggests a peripheral neuropathy; difficulty with bowel and/or bladder control suggests a myelopathy or cauda equina syndrome)
  • MRI is the usually the best imaging modality
    –Acute paraplegia/paraparesis is suggestive of an acute myelopathy or polyradiculopathy, and prompt imaging is required to identify surgically treatable lesions
  • EMG/nerve conduction studies to evaluate for possible neuropathy, polyradiculopathy, or myopathy
  • CSF examination may show signs of infection, elevated protein in Guillain-Barré syndrome, or findings consistent with multiple sclerosis (e.g., oligoclonal bands)
  • Laboratory testing may include CBC, electrolytes, calcium, glucose, ESR, vitamin B₁₂, folate, ANA
  • DNA testing is available for many of the inherited ataxias
  • Genetic testing

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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

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Source: In a Page: Signs and Symptoms, 2004

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

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

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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.

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Source: Differential Diagnosis in Primary Care, 2007

EXTREMITY MASS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

If the lesion is suspected to arise in the skin, simple biopsy or excision is the best approach. Deeper masses require careful examination, x-rays of the bones and soft tissue, bone scans, CT scans, ultrasonographic studies, and phlebography, arteriography, or lymphangiography. Surgical exploration of the area may be the only means to accomplish a specific diagnosis.

Approach to the Diagnosis

Because the extremities are not considered vital areas, the primary method of diagnosing the cause of a mass is exploration and biopsy. This is all well and good when the lesion is on the skin or subcutaneous tissue; however, when the mass is in the deeper tissues, it is wise to utilize diagnostic test to determine what the mass is before exploration. If the mass is suspected to be a varix or aneurysm, ultrasonography can be extremely useful in defining it. If the mass is attached to or thought to originate in bone, x-rays of the area and bone scans are useful. If it is uncertain what tissue the mass originates from, a CT scan can be used to help define it. Before ordering any of the above tests, it is best to consult a general or orthopedic surgeon to help select the most appropriate test for the case at hand.

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Source: Differential Diagnosis in Primary Care, 2007

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

After you’re satisfied that the patient’s spine and respiratory status are stabilized — or if the analgesia isn’t severe and isn’t accompanied by signs of spinal cord injury — perform a physical examination and baseline neurologic evaluation. First, take the patient’s vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech, gag reflex, and ability to swallow.

If possible, observe the patient’s gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 38 and 39.) Also, test temperature sensation over all dermatomes, using two test tubes — one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes. Check for increased muscle tone by extending and flexing the patient’s elbows and knees as he tries to relax.

Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma — a fall, sports injury, or automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family.

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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.

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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.

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

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

Once you’re satisfied that the patient’s spine and respiratory status are stabilized—or if the analgesia isn’t severe and isn’t accompanied by signs of spinal cord injury—perform a physical examination and baseline neurologic evaluation. First, take the patient’s vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech and ability to swallow.

If possible, observe the patient’s gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 48 and 49.) Also, test temperature sensation over all dermatomes, using two test tubes—one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes (DTRs). Check for increased muscle tone by extending and flexing the patient’s elbows and knees as he tries to relax.

Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma, such as a fall, a sports injury, or an automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family.

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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.

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

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.

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Source: Handbook of Diseases, 2003

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

After assuring spinal cord stabilization, proceed with assessing the patient. Establish the onset of analgesia (sudden or gradual). Did the patient suffer recent trauma, such as a fall, sports injury, or automobile accident?  Obtain a complete medical history, noting incidence of cancer in the patient or his family.

Physical examination

Assess the patient’s vital signs, including the pattern of respirations. Determine his level of consciousness. Assist to test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his ability to swallow.

Assist to perform a full neurologic assessment, including orientation to person, place, and time. Assess the patient’s ability to speak clearly, pupil size and reaction to light, ability to follow commands, ability to wiggle extremities, and awareness of touch. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough assessment of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 18 and 19.) Assess the patient’s temperature sensation over all dermatomes, using two test tubes — one filled with warm water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes (DTRs). Check for increased muscle tone by extending and flexing the patient’s elbows and knees as he tries to relax.

After a spinal cord injury is ruled out, observe the patient’s gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities.

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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.

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

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

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

After you're satisfied that the patient's spine and respiratory status are stabilized—or if the analgesia isn't severe and isn't accompanied by signs of spinal cord injury—perform a physical examination and baseline neurologic evaluation. First, take the patient's vital signs and assess his level of consciousness. Then test pupillary, corneal, cough, and gag reflexes to rule out brain stem and cranial nerve involvement. If the patient is conscious, evaluate his speech, gag reflex, and ability to swallow.

If possible, observe the patient's gait and posture and assess his balance and coordination. Evaluate muscle tone and strength in all extremities. Test for other sensory deficits over all dermatomes (individual skin segments innervated by a specific spinal nerve) by applying light tactile stimulation with a tongue depressor or cotton swab. Perform a more thorough check of pain sensitivity, if necessary, using a pin. (See Testing for analgesia, pages 32 and 33.)

Test temperature sensation over all dermatomes, using two test tubes—one filled with hot water, the other with cold water. In each arm and leg, test vibration sense (using a tuning fork), proprioception, and superficial and deep tendon reflexes. Check for increased muscle tone by extending and flexing the patient's elbows and knees as he tries to relax. Focus your history taking on the onset of analgesia (sudden or gradual) and on any recent trauma—a fall, sports injury, or automobile accident. Obtain a complete medical history, noting especially any incidence of cancer in the patient or his family. Obtain a complete drug history.

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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.

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Source: Nursing: Interpreting Signs and Symptoms, 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.

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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.

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Source: Differential Diagnosis in Primary Care, 2007

EXTREMITY MASS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

If the lesion is suspected to arise in the skin, simple biopsy or excision is the best approach. Deeper masses require careful examination, x-rays of the bones and soft tissue, bone scans, CT scans, ultrasonographic studies, and phlebography, arteriography, or lymphangiography. Surgical exploration of the area may be the only means to accomplish a specific diagnosis.

Approach to the Diagnosis

Because the extremities are not considered vital areas, the primary method of diagnosing the cause of a mass is exploration and biopsy. This is all well and good when the lesion is on the skin or subcutaneous tissue; however, when the mass is in the deeper tissues, it is wise to utilize diagnostic tests to determine what the mass is before exploration. If the mass is suspected to be a varix or aneurysm, ultrasonography can be extremely useful in defining it. If the mass is attached to or thought to originate in bone, x-rays of the area and bone scans are useful. If it is uncertain what tissue the mass originates from, a CT scan can be used to help define it. Before ordering any of the above tests, it is best to consult a general or orthopedic surgeon to help select the most appropriate test for the case at hand.

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Source: Differential Diagnosis in Primary Care, 2007

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