Causes of Adrenoleukodystrophy
Adrenoleukodystrophy Causes: Book Excerpts
Adrenoleukodystrophy as a symptom:
Conditions listing Adrenoleukodystrophy
as a symptom may also be potential underlying causes of Adrenoleukodystrophy.
Our database lists the following as having
Adrenoleukodystrophy as a symptom of that condition:
Related information on causes of Adrenoleukodystrophy:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Adrenoleukodystrophy may be found in:
Causes of Adrenoleukodystrophy: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Adrenoleukodystrophy.
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)
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Muscle spasticity [Muscle hypertonicity]:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Amyotrophic lateral sclerosis (ALS)
ALS commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), and a positive Babinski’s sign. Earlier effects include progressive muscle weakness and flaccidity that typically begin in the hands and arms and eventually spread to the trunk, neck, larynx, pharynx, and legs; progressive respiratory muscle weakness leads to respiratory insufficiency. Other findings include dysphagia, dysarthria, excessive drooling, and depression.
Epidural hemorrhage
With epidural hemorrhage, bilateral limb spasticity is a late and ominous sign. Other findings include a momentary loss of consciousness after head trauma, followed by a lucid interval and then a rapid deterioration in the level of consciousness (LOC). The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; a high fever; a decreased and bounding pulse; a widened pulse pressure; elevated blood pressure; an irregular respiratory pattern; and decerebrate posture. A positive Babinski’s sign can be elicited.
Spinal cord injury
Spasticity commonly results from cervical and high thoracic spinal cord injury, especially from incomplete lesions. Spastic paralysis in the affected limbs follows initial flaccid paralysis; typically, spasticity and muscle atrophy increase for up to 1¼ to 2 years after the injury, and then gradually regress to flaccidity. Associated signs and symptoms vary with the level of injury, but may include respiratory insufficiency or paralysis, sensory losses, bowel and bladder dysfunction, hyperactive DTRs, a positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.
Stroke
Spastic paralysis may develop on the affected side following the acute stage of a stroke. Associated findings vary with the site and extent of vascular damage and may include dysarthria, aphasia, ataxia, apraxia, agnosia, ipsilateral paresthesia or sensory loss, vision disturbances, an altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, a headache, vomiting, and seizures.
Tetanus
Tetanus is a rare, life-threatening disease that produces varying degrees of spasticity. In generalized tetanus — the most common form — early signs and symptoms include painful jaw and neck stiffness, trismus, a headache, irritability, restlessness, a low-grade fever with chills, tachycardia, diaphoresis, and hyperactive DTRs. As the disease progresses, painful involuntary spasms may spread and cause boardlike abdominal rigidity, opisthotonos, and a characteristic grotesque grin known as risus sardonicus. Reflex spasms may occur in any muscle group with the slightest stimulus. Glottal, pharyngeal, or respiratory muscle involvement can cause death by asphyxia or cardiac failure.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Gait, spastic [Hemiplegic gait]:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Brain abscess
In brain abscess, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): a headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, visual disturbances, nystagmus, and pupillary inequality. The patient’s level of consciousness may range from drowsiness to stupor.
Brain tumor
Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (a headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.
Head trauma
Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, a headache, and focal neurologic signs, such as aphasia and visual field deficits.
Multiple sclerosis
Spastic gait begins insidiously and follows multiple sclerosis’ characteristic cycle of remission and exacerbation. The gait, as well as other signs and symptoms, commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include facial pain, paresthesia, incoordination, loss of proprioception and vibration sensation in the ankle and toes, and vision disturbances.
Stroke
Spastic gait usually appears after a period of muscle weakness and hypotonicity on the affected side. Associated effects may include unilateral muscle atrophy, sensory loss, and footdrop; aphasia; dysarthria; dysphagia; visual field deficits; diplopia; and ocular palsies.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Adrenal hypofunction:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Adrenal hypofunction occurs when more than 90% of both adrenal glands are destroyed, an occurrence that typically results from an autoimmune process in which circulating antibodies react specifically against the adrenal tissue. Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (acquired immunodeficiency syndrome, histoplasmosis, and cytomegalovirus). Rarely, a familial tendency to autoimmune disease predisposes the patient to adrenal hypofunction and other endocrinopathies.
Secondary adrenal hypofunction that results in glucocorticoid deficiency can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or removal of a nonendocrine, corticotropin-secreting tumor. Adrenal crisis follows when trauma, surgery, or other physiologic stress exhausts the body’s stores of glucocorticoids in a person with adrenal hypofunction.
Adrenal hypofunction affects 1 in 16,000 neonates congenitally. In adults, it affects 8 in 100,000 people, and males and females are affected equally. There’s no racial predilection.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Creutzfeldt-Jakob disease:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The causative organism is difficult to identify because no foreign ribonucleic acid or deoxyribonucleic acid has been linked to the disease. CJD is believed to be caused by a specific protein called a prion, which lacks nucleic acids, resists proteolytic digestion, and spontaneously aggregates in the brain. Most cases are sporadic; 5% to 15% are familial, with an autosomal dominant pattern of inheritance. Although CJD isn’t transmitted by normal casual contact, human-to-human transmission can occur as a result of certain medical procedures, such as corneal and cadaveric dura mater grafts. Isolated cases are attributed to treatment during childhood with human growth hormone and to improperly decontaminated neurosurgical instruments and brain electrodes.
CJD generally affects adults ages 40 to 65 and occurs in more than 50 countries. Males and females are affected equally. In people younger than age 30, incidence is 5 in 1,000,000,000; in all other age groups, incidence is 1 in 1,000,000.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
West Nile encephalitis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
WNV is transmitted to humans by the bite of a mosquito (primarily the Culex species) infected with the virus. It's considered the primary vector for WNV and the source of the August 1999 outbreak in New York, New Jersey and Connecticut. Mosquitoes become infected by feeding on birds contaminated with the West Nile virus and then transmitting it to humans and animals during a blood meal or “bite.” (See Transmission routes of West Nile virus, page 256.)
Ticks have been found infected with WNV in Africa and Asia only. The role of ticks in the transmission and maintenance of the virus remains uncertain, and to date they aren't considered vectors for WNV in the United States.
The Centers for Disease Control and Prevention has reported that there is no evidence that a person can contract the virus from handling live or dead infected birds. However, avoid barehanded contact when handling dead animals, including birds, and use gloves or double plastic bags to dispose of a carcass. Report the finding to the local health department.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Skin, bronze:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Adrenal hyperplasia
The skin assumes a dark bronze tone within a few months. Other findings include visual field deficits and headache (from an expanding pituitary lesion), and signs of masculinization in females.
Biliary cirrhosis
This disorder causes bronze skin from melanosis of exposed areas of jaundiced skin: eyelids, palms, neck, and chest or back. The patient may also experience generalized pruritus, weakness, fatigue, jaundice, dark urine, pale stools with steatorrhea, decreased appetite with weight loss, and hepatomegaly.
Chronic renal failure
The skin becomes pallid, yellowish bronze, dry, and scaly. Other findings include ammonia breath odor, oliguria, fatigue, decreased mental acuity, seizures, muscle cramps, peripheral neuropathy, bleeding tendencies, pruritus and, occasionally, uremic frost and hypertension.
Hemochromatosis
An early sign is progressive, generalized bronzing accentuated by metallic gray-bronze skin on sun-exposed areas, genitalia, and scars. Mucous membranes are affected less often. Early associated effects include weakness, lethargy, weight loss, abdominal pain, loss of libido, polydipsia, and polyuria.
Malnutrition
As weight loss depletes body nutrients, bronzing develops along with apathy, lethargy, anorexia, weakness, and slow pulse and respiratory rates. Patients may develop paresthesia in the extremities; dull, sparse, dry hair; brittle nails; dark, swollen cheeks; dry, flaky skin; red, swollen lips; muscle wasting; and gonadal atrophy in males.
Primary adrenal insufficiency
Bronze skin is a classic sign. Other findings include axillary and pubic hair loss, vitiligo, progressive fatigue, weakness, anorexia, nausea and vomiting, weight loss, orthostatic hypotension, weak and irregular pulse, abdominal pain, irritability, diarrhea or constipation, amenorrhea, and syncope.
Wilson’s disease
Kayser-Fleischer rings—rusty brown rings of pigment around the corneas—characterize this disease, which may cause skin bronzing. Other effects include incoordination, dysarthria, chorea, ataxia, muscle spasms and rigidity, abdominal distress, fatigue, personality changes, hypotension, syncope, and seizures.
Other causes
Drugs
Prolonged therapy with high doses of a phenothiazine may cause gradual bronzing of the skin.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Muscle spasticity [Muscle hypertonicity]:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Amyotrophic lateral sclerosis
This disorder commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes, and a positive Babinski’s sign. Earlier effects include progressive muscle weakness and flaccidity that typically begin in the hands and arms and eventually spread to the trunk, neck, larynx, pharynx, and legs; progressive respiratory muscle weakness leads to respiratory insufficiency. Other findings include dysphagia, dysarthria, excessive drooling, and depression.
Epidural hemorrhage
With this disorder, bilateral limb spasticity is a late and ominous sign. Other findings include a momentary loss of consciousness after head trauma, followed by a lucid interval and then a rapid deterioration in level of consciousness. The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; high fever; decreased and bounding pulse; widened pulse pressure; elevated blood pressure; irregular respiratory pattern; and decerebrate posture. A positive Babinski’s sign can be elicited.
Multiple sclerosis
Muscle spasticity, hyperreflexia, and contractures may eventually develop; earlier muscle changes include progressive weakness and atrophy. Associated signs and symptoms typically wax and wane and may include diplopia, blurring or loss of vision, nystagmus, sensory loss or paresthesia, dysarthria, dysphagia, incoordination, ataxic gait, intention tremors, emotional lability, impotence, and urinary dysfunction.
Spinal cord injury
Spasticity commonly results from cervical and high thoracic spinal cord injury, especially from incomplete lesions. Spastic paralysis in the affected limbs follows initial flaccid paralysis; typically, spasticity and muscle atrophy increase for up to 1¼ to 2 years after the injury, then gradually regress to flaccidity. Associated signs and symptoms vary with the level of injury but may include respiratory insufficiency or paralysis, sensory losses, bowel and bladder dysfunction, hyperactive deep tendon reflexes, positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.
Stroke
Spastic paralysis may develop on the affected side following the acute stage of a stroke. Associated findings vary with the site and extent of vascular damage and may include dysarthria, aphasia, ataxia, apraxia, agnosia, ipsilateral paresthesia or sensory loss, visual disturbance, altered level of consciousness, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.
Tetanus
This rare, life-threatening disease produces varying degrees of spasticity. In generalized tetanus, the most common form, early signs and symptoms include painful jaw and neck stiffness, trismus, headache, irritability, restlessness, low-grade fever with chills, tachycardia, diaphoresis, and hyperactive deep tendon reflexes. As the disease progresses, painful involuntary spasms may spread and cause boardlike abdominal rigidity, opisthotonos, and a characteristic grotesque grin known as risus sardonicus. Reflex spasms may occur in any muscle group with the slightest stimulus. Glottal, pharyngeal, or respiratory muscle involvement can cause death by asphyxia or cardiac failure.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Gait, spastic [Hemiplegic gait]:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Brain abscess
In this disorder, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, visual disturbances, nystagmus, and pupillary inequality. The patient’s level of consciousness may range from drowsiness to stupor.
Brain tumor
Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.
Head trauma
Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, headache, and focal neurologic signs, such as aphasia and visual field deficits.
Multiple sclerosis (MS)
Spastic gait begins insidiously and follows this disorder’s characteristic cycle of remission and exacerbation. Like other signs and symptoms of MS, the gait commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include vision disturbances, facial pain, paresthesia, incoordination, and loss of proprioception and vibration sensation in the ankle and toes.
Stroke
Spastic gait usually appears after a period of muscle weakness and hypotonicity on the affected side. Associated effects may include unilateral muscle atrophy, sensory loss, and footdrop; aphasia; dysarthria; dysphagia; visual field deficits; diplopia; and ocular palsies.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Peripheral Neuropathy:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Diabetes
❑ Alcohol
❑ Vitamin B12 deficiency
❑ Drugs
❑ Carcinomatous
❑ Lead
❑ Guillain-Barré
❑ Tabes dorsalis
❑ Syringomyelia
❑ Polyarteritis nodosa
❑ Amyloidosis
❑ Polymyositis
❑ Pellagra
❑ Arsenic
❑ Porphyria
❑ Wallenberg syndrome
❑ Thalamic lesion
❑ Brown-Sequard syndrome
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Adrenal hypofunction:
Causes
(Handbook of Diseases)
The following are causes of primary and secondary adrenal hypofunction and adrenal crisis.
Primary hypofunction
Addison’s disease occurs when more than 90% of both adrenal glands are destroyed. Such destruction usually results from an autoimmune process (autoimmune adrenalitis) in which circulating antibodies react specifically against the adrenal tissue.
CLINICAL TIP: Suspect adrenal insufficiency in patients with acquired immunodeficiency syndrome. Although symptoms may not be present, testing frequently reveals abnormal results.
Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (histoplasmosis, cytomegalovirus). Rarely, a family history of autoimmune disease predisposes the patient to Addison’s disease and other endocrinopathies.
Secondary hypofunction
Secondary hypofunction, which results in glucocorticoid deficiency, can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or the removal of a corticotropin-secreting tumor.
Adrenal crisis
After trauma, surgery, or other physiologic stress, adrenal crisis exhausts the body’s stores of glucocorticoids in a person with adrenal hypofunction.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Creutzfeldt-Jakob disease:
Causes
(Handbook of Diseases)
The causative organism is difficult to identify because no foreign ribonucleic acid or deoxyribonucleic acid has been linked to the disease. CJD is believed to be caused by a specific protein called a prion, which lacks nucleic acids, resists proteolytic digestion, and spontaneously aggregates in the brain. Most cases are sporadic; 5% to 15% are familial, with an autosomal dominant pattern of inheritance. Although CJD isn’t transmitted by normal casual contact, human-to-human transmission can occur as a result of certain medical procedures, such as corneal and cadaveric dura mater grafts. Isolated cases are attributed to treatment during childhood with human growth hormone and to improperly decontaminated neurosurgical instruments and brain electrodes.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Encephalitis:
Causes
(Handbook of Diseases)
Encephalitis generally results from infection with arboviruses specific to rural areas. In urban areas, it’s most frequently caused by enteroviruses (coxsackievirus, poliovirus, and echovirus).
Other causes include herpesvirus, mumps virus, human immunodeficiency virus, adenoviruses, and demyelinating diseases after measles, varicella, rubella, or vaccination.
Between World War I and the Depression, a type of encephalitis known as lethargic encephalitis, von Econ-omo’s disease, or sleeping sickness occurred with some regularity. The causative virus was never clearly identified, and the disease is rare today. Even so, the term sleeping sickness persists and in many cases is mistakenly used to describe other types of encephalitis as well. The most recent outbreak of mosquito-borne encephalitis was West Nile encephalitis.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
West Nile encephalitis:
Causes
(Handbook of Diseases)
WNV is transmitted to humans by the bite of an infected mosquito (primarily the Culex species). Mosquitoes become infected by feeding on infected birds.
Ticks infected with WNV have been found in Africa and Asia, but their role in transmission and maintenance of the virus is uncertain; they aren’t considered vectors for WNV in the United States.
The Centers for Disease Control and Prevention has reported that there’s no evidence that a person can contract the virus from handling live or dead infected birds. However, barehanded contact when handling dead animals, including dead birds, should be avoided; if a dead animal must be handled, gloves or other protective measures should be used to dispose of the carcass. A dead bird is a sign that there may be infected mosquitoes in the area; findings should be reported to the nearest Emergency Management Office.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Skin, bronze:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Adrenal hyperplasia
With adrenal hyperplasia, the skin assumes a dark bronze tone within a few months. Other findings include visual field deficits and headache (from an expanding pituitary lesion), and signs of masculinization in females such as clitoral enlargement, and male distribution of hair, fat, and muscle mass.
Biliary cirrhosis
Biliary cirrhosis causes bronze skin from melanosis of exposed areas of jaundiced skin: eyelids, palms, neck, and chest or back. The patient may also experience generalized pruritus, weakness, fatigue, jaundice, dark urine, pale stools with steatorrhea, decreased appetite with weight loss, and hepatomegaly.
Hemochromatosis
An early sign of hemochromatosis is progressive, generalized bronzing accentuated by metallic gray-bronze skin on sun-exposed areas, genitalia, and scars. Mucous membranes are affected less often. Early associated effects include weakness, lethargy, weight loss, abdominal pain, loss of libido, polydipsia, and polyuria.
CULTURAL CUE:Hereditary hemochromatosis is the most common genetic disorder in whites, affecting 1 in 200 to 300 people of Northern European descent.
Malnutrition
As weight loss, which occurs from malnutrition, depletes body nutrients, bronzing develops along with apathy, lethargy, anorexia, weakness, and slow pulse and respiratory rates. Patients may develop paresthesia in the extremities; dull, sparse, dry hair; brittle nails; dark, swollen cheeks; dry, flaky skin; red, swollen lips; muscle wasting; and gonadal atrophy in males.
Primary adrenal insufficiency
Bronze skin is a classic sign of primary adrenal insufficiency. Other findings include axillary and pubic hair loss, vitiligo, progressive fatigue, weakness, anorexia, nausea and vomiting, weight loss, orthostatic hypotension, weak and irregular pulse, abdominal pain, irritability, diarrhea or constipation, amenorrhea, and syncope.
Renal failure (chronic)
With chronic renal failure, the skin becomes pallid, yellowish bronze, dry, and scaly. Other findings include ammonia breath odor, oliguria, fatigue, decreased mental acuity, seizures, muscle cramps, peripheral neuropathy, bleeding tendencies, pruritus and, occasionally, uremic frost and hypertension.
Other causes
Drugs
Prolonged therapy with high doses of a phenothiazine may cause gradual bronzing of the skin.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Muscle spasticity:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), and a positive Babinski’s sign. Earlier effects include progressive muscle weakness and flaccidity that typically begin in the hands and arms and eventually spread to the trunk, neck, larynx, pharynx, and legs. Progressive respiratory muscle weakness leads to respiratory insufficiency. Other findings include dysphagia, dysarthria, excessive drooling, and depression.
Epidural hemorrhage
Bilateral limb spasticity is a late and ominous sign of epidural hemorrhage. Other findings include a momentary loss of consciousness after head trauma, followed by a lucid interval and then a rapid deterioration in level of consciousness (LOC). The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; high fever; decreased and bounding pulse; widened pulse pressure; elevated blood pressure; irregular respiratory pattern; and decerebrate posture. A positive Babinski’s sign can be elicited.
Multiple sclerosis
Muscle spasticity, hyperreflexia, and contractures may eventually develop in patients with multiple sclerosis; earlier muscle changes include progressive weakness and atrophy. Associated signs and symptoms typically wax and wane and may include diplopia, blurring or loss of vision, nystagmus, sensory loss or paresthesia, dysarthria, dysphagia, incoordination, ataxic gait, intention tremors, emotional lability, impotence, and urinary dysfunction.
Spinal cord injury
Spasticity commonly results from cervical and high thoracic spinal cord injury, especially from incomplete lesions. Spastic paralysis in the affected limbs follows initial flaccid paralysis; typically, spasticity and muscle atrophy increase for up to 2 years after the injury, then gradually regress to flaccidity. Associated signs and symptoms vary with the level of injury but may include respiratory insufficiency or paralysis, sensory losses, bowel and bladder dysfunction, hyperactive DTRs, positive Babinski’s sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.
Stroke
Spastic paralysis may develop on the affected side following the acute stage of a stroke. Associated findings vary with the site and extent of vascular damage and may include dysarthria, aphasia, ataxia, apraxia, agnosia, ipsilateral paresthesia or sensory loss, visual disturbance, altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Muscle spasticity [Muscle hypertonicity]:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Amyotrophic lateral sclerosis (ALS).ALS commonly produces spasticity, spasms, coarse fasciculations, hyperactive deep tendon reflexes (DTRs), and a positive Babinski's sign. Earlier effects include progressive muscle weakness and flaccidity that typically begin in the hands and arms and eventually spread to the trunk, neck, larynx, pharynx, and legs; progressive respiratory muscle weakness leads to respiratory insufficiency. Other findings include dysphagia, dysarthria, excessive drooling, and depression.
Epidural hemorrhage.With epidural hemorrhage, bilateral limb spasticity is a late and ominous sign. Other findings include a momentary loss of consciousness after head trauma, followed by a lucid interval and then a rapid deterioration in the level of consciousness (LOC). The patient may also develop unilateral hemiparesis or hemiplegia; seizures; fixed, dilated pupils; a high fever; a decreased and bounding pulse; a widened pulse pressure; elevated blood pressure; an irregular respiratory pattern; and decerebrate posture. A positive Babinski's sign can be elicited.
Spinal cord injury.Muscle spasticity commonly results from cervical and high thoracic spinal cord injury, especially from incomplete lesions. Spastic paralysis in the affected limbs follows initial flaccid paralysis; typically, spasticity and muscle atrophy increase for up to 11⁄2 to 2 years after the injury, and then gradually regress to flaccidity. Associated signs and symptoms vary with the level of injury, but may include respiratory insufficiency or paralysis, sensory losses, bowel and bladder dysfunction, hyperactive DTRs, a positive Babinski's sign, sexual dysfunction, priapism, hypotension, anhidrosis, and bradycardia.
Stroke.Spastic paralysis may develop on the affected side following the acute stage of a stroke. Associated findings vary with the site and extent of vascular damage and may include dysarthria, aphasia, ataxia, apraxia, agnosia, ipsilateral paresthesia or sensory loss, vision disturbances, altered LOC, amnesia and poor judgment, personality changes, emotional lability, bowel and bladder dysfunction, headache, vomiting, and seizures.
Tetanus.Tetanus is a rare, life-threatening disease that produces varying degrees of muscle spasticity. In generalized tetanus—the most common form—early signs and symptoms include painful jaw and neck stiffness, trismus, headache, irritability, restlessness, a low-grade fever with chills, tachycardia, diaphoresis, and hyperactive DTRs. As the disease progresses, painful involuntary spasms may spread and cause boardlike abdominal rigidity, opisthotonos, and a characteristic grotesque grin known as risus sardonicus. Reflex spasms may occur in any muscle group with the slightest stimulus. Glottal, pharyngeal, or respiratory muscle involvement can cause death by asphyxia or cardiac failure.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Gait, spastic [Hemiplegic gait]:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Brain abscess.In brain abscess, spastic gait generally develops slowly after a period of muscle flaccidity and fever. Early signs and symptoms of abscess reflect increased intracranial pressure (ICP): a headache, nausea, vomiting, and focal or generalized seizures. Later, site-specific features may include hemiparesis, tremors, vision disturbances, nystagmus, and pupillary inequality. The patient's level of consciousness may range from drowsiness to stupor.
Brain tumor.Depending on the site and type of tumor, spastic gait usually develops gradually and worsens over time. Accompanying effects may include signs of increased ICP (a headache, nausea, vomiting, and focal or generalized seizures), papilledema, sensory loss on the affected side, dysarthria, ocular palsies, aphasia, and personality changes.
Head trauma.Spastic gait typically follows the acute stage of head trauma. The patient may also experience focal or generalized seizures, personality changes, a headache, and focal neurologic signs, such as aphasia and visual field deficits.
Multiple sclerosis.Spastic gait begins insidiously and follows multiple sclerosis' characteristic cycle of remission and exacerbation. The gait, as well as other signs and symptoms, commonly worsens in warm weather or after a warm bath or shower. Characteristic weakness, usually affecting the legs, ranges from minor fatigability to paraparesis with urinary urgency and constipation. Other effects include facial pain, paresthesia, incoordination, loss of proprioception and vibration sensation in the ankle and toes, and vision disturbances.
Stroke.With a stroke, spastic gait usually appears after a period of muscle weakness and hypotonicity on the affected side. Associated effects may include unilateral muscle atrophy, sensory loss, and footdrop; aphasia; dysarthria; dysphagia; visual field deficits; diplopia; and ocular palsies.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Encephalitis:
Encephalitis - pathophysiology
(The 5-Minute Pediatric Consult)
- Direct or delayed (postinfectious) reaction by the immune system to a virus, bacteria, fungus, or parasite
- Organisms enter the CNS via the systemic circulation, direct inoculation (trauma), or neural pathways (rabies, herpes simplex virus [HSV]).
- Infiltration/activation of inflammatory cells in the CNS with release of cytokines
- Inclusion bodies (intranuclear, HSV, subacute sclerosing panencephalitis [SSPE], viral, intracytoplasmic, rabies); CSF; and serological changes
Encephalitis - etiology
- The most common causes of encephalitis are viruses:
- Summer (enteroviruses)
- Summer and fall (western and eastern equine, St. Louis, La Crosse, and West Nile encephalitis)
- Winter (varicella)
- Nonviral causes (tuberculosis, Lyme disease, toxoplasmosis, cat scratch disease, rickettsial disease, tick-borne infections) are sometimes associated with specific environmental or geographic exposure.
- The most common cause of sporadic encephalitis is HSV (rabies and HIV also occur in all seasons).
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Source: The 5-Minute Pediatric Consult, 2008
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