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127 Cards in this Set
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Spastic and flaccid paralysis
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Amyotrophic lateral sclerosis (ALS)
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Tracts Affected=Corticospinal tract, ventral horn
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Flaccid paralysis
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Poliomyelitis
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Tracts Affected=Ventral horn
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Impaired proprioception, pain
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Tabes dorsalis
(tertiary syphilis) |
Tracts Affected=Dorsal columns
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Bilateral loss of pain and temperature (one level below lesion), bilateral spastic paresis (below lesion), bilateral flaccid paralysis (level of lesion)
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Spinal artery syndrome
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Tracts Affected=Corticospinal tract, spinothalamic tract,
ventral horn, lateral gray matter (dorsal columns spared) |
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Bilateral loss of vibration and discrimination and bilateral spastic paresis affecting legs before arms
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Vitamin B12 deficiency
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Tracts Affected=Dorsal columns, corticospinal tract
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Bilateral loss of pain and temperature (one level below lesion), bilateral flaccid paralysis (level of lesion)
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Syringomyelia
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Tracts Affected=Ventral horn, ventral white commissure
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Ipsilateral loss of vibration and discrimination (below lesion), ipsilateral spastic paresis (below lesion), ipsilateral flaccid paralysis (level of lesion), contralateral loss of pain and temperature (below lesion)
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Brown-Séquard syndrome
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Tracts Affected=All tracts on one side of cord
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H/P=Headache, neck pain, photophobia, malaise, vomiting, confusion; fever. Brudzinski's sign (i.e., neck flexion in supine patient prompts reflexive hip flexion) and Kernig's sign (i.e., painful knee extension occurs with hip flexion in supine patient) are not reliable tests
Petechiae are seen in Neisseria meningitidis infection Change in mental status, seizures, decreased consciousness seen with worsening infection Symptoms in children may be nonfocal |
Bacterial meningitis
Infection of meningeal tissue in brain or spinal cord Infection is usually caused by hematogenous spread, local extension, or cerebral spinal fluid (CSF) exposure to bacteria (e.g., neurosurgery) Risk factors = ear infection, sinusitis, immunocompromise, neurosurgery, maternal group β-streptococci infection during birth Complications = seizures, increased ICP, subdural effusion, empyema, brain abscess, hearing loss, mental impairment |
Labs = increased white blood cell count (WBC); blood cultures frequently positive; lumbar puncture (LP) useful for differentiating causes of meningitis from each other and from healthy patients; CSF culture may determine exact agent
Radiology = computed tomography (CT) or magnetic resonance imaging (MRI) may be helpful for ruling out other pathologies Treatment = initially cephalosporins (3rd generation) until specific agent is identified, then agent-specific antibiotics; close contacts of patient should be given rifampin for prophylaxis in cases of Neisseria infection and for H. influenzae infection in children without prior vaccination |
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H/P = nausea, vomiting, headache, neck pain, photophobia, malaise; fever, rash; symptoms generally milder than for bacterial meningitis
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Viral meningitis (aseptic meningitis)
Meningitis caused by viral infection by enterovirus, echovirus, herpes simplex virus, lymphocytic choriomeningitis virus, mumps virus |
Labs = LP helpful for diagnosis; viral culture will confirm etiology
Treatment = empiric antibiotics may be started until viral cause is confirmed; supportive care usually sufficient for confirmed viral cases |
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H/P =
Malaise, headache, vomiting, neck pain, decreased consciousness; change in mental status, focal neurologic deficits (e.g., hemiparesis, pathologic reflexes, nerve palsy), fever Skin lesions seen with herpes simplex virus Parotid swelling seen with mumps Flaccid paralysis with maculopapular rash seen in West Nile virus |
Inflammation of brain parenchyma caused by viral infection (e.g., varicella-zoster virus, herpes simplex virus, mumps virus, poliovirus, rhabdovirus, Coxsackie virus, arbovirus, flavivirus, measles) or immunologic response to viral infection
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Labs =
LP shows increased WBCs, normal glucose Culture generally not reliable Serologic testing may be useful to identify viral cause Brain biopsy can provide definitive diagnosis but is generally impractical Radiology = CT or MRI may show inflamed region of brain with effusion Treatment = maintain normal ICP, supportive care; herpes simplex virus treated with acyclovir |
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H/P = headache, neck pain, nausea, vomiting, malaise; fever, change in mental status, focal neurologic deficits, papilledema, seizures
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Brain abscess
Collection of pus in brain parenchyma resulting from extension of local bacterial infection, head wound, or hematogenous spread of bacteria |
Labs = brain biopsy or culture of abscess material performed during surgical drainage can be used to confirm bacterial identity
Radiology = MRI or CT may localize lesion; CT-guided biopsy can be performed to collect material for culture Treatment = empiric antibiotics until specific agent identified, corticosteroids, surgical drainage |
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H/P = possibly asymptomatic; headache, neck pain, vomiting, sore throat; fever, Normal sensation, muscle weaknesS that may progress to paralysis in severe cases
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Poliomyelitis
Poliovirus (a picornavirus) infection of brain and motor neurons |
Labs = positive polio-specific antibody; LP consistent with viral meningitis; viral culture helpful for diagnosis
Treatment = with supportive care, most patients recover fully; assisted respiration may be required if respiratory muscles are affected |
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H/P = malaise, headache, restlessness, Fear of water ingestioN (secondary to laryngeal spasm); progressive cases exhibit severe central nervous system (CNS) excitability, Foaming at moutH, very painful laryngeal spasms, Alternating mania and stupoR
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Rabies
Rhabdovirus transmitted to humans by bite of infected animal Causes severe encephalitis with neuronal degeneration and inflammation |
Labs =
Suspected animal should be caught and tested or observed for signs of rabies If animal appears to be infected, it should be killed and the brain should be tested for presence of virus and Negri bodies (i.e., round eosinophilic inclusions in neurons) Viral testing in humans (CSF, skin, serum) with symptoms is confirmatory of disease Treatment = clean wound area thoroughly; administer rabies immunoglobulin and vaccine to patient if animal was infected or if rabies suspicion is high |
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H/P = sudden severe pain in distributions of maxillary and mandibular branches; “trigger zone” stimulation may induce pain
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Trigeminal neuralgia
Head and facial pain in trigeminal nerve distribution possibly caused by compression or irritation of trigeminal nerve root |
Radiology = MRI may identify lesions related to nerve compression
Treatment = carbamazepine, baclofen, phenytoin, gabapentin, valproate, clonazepam, or other anticonvulsants; surgical decompression of nerve may be helpful |
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Headache 4–72 hr
10–30 yr of age, female > male Unilateral, throbbing Nausea, vomiting, preceding aura (visual abnormalities), photophobia |
Migraine
likely due to neuronal dysfunction precipitated by Stress, oral contraceptives, menstruation, exertion, foods containing tyramine or nitrates (chocolate, cheese, processed meats) POUND: pounding, one-day duration, unilateral, nausea, disability |
Treatment=NSAIDs, ergots, sumatriptan; IV antiemetics useful for severe cases; prophylaxis includes tricyclic antidepressants, β-blockers, calcium channel blockers, ergots
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Headache 30 min–3 hr
Young men Severe, unilateral, periorbital, recurrent (“in clusters” over time) Horner's syndrome (ptosis, myosis, anhidrosis), lacrimation, nasal congestion |
Cluster Headache
likely extracerebral cause precipitated by Alcohol, vasodilators |
Treatment=100% O2, ergots, sumatriptan; prophylaxis similar to that for migraines
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Headache Variable
Bilateral, tightness, occipital or neck pain Anxiety |
Tension Headache
Female > male precipitated by Stress, fatigue NOT disabled during |
Treatment=NSAIDs, ergots, sumatriptan, relaxation exercises
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H/P =
Sudden appearance of focal neurologic deficits, including weakness, paresthesias, brief unilateral blindness (i.e., amaurosis fugax) or other vision abnormality, impaired coordination, vertigo Carotid bruits suggest carotid atherosclerosis Harsh systolic murmur suggests aortic stenosis Risk factors = hypertension (HTN), diabetes mellitus (DM), coronary artery disease (CAD), tobacco, hyperlipidemia, hypercoagulable states |
Transient ischemic attack (TIA)
Acute focal neurologic deficits that last >24 hr and are caused by temporarily impaired vascular supply to brain (e.g., emboli, aortic stenosis, vascular spasm) Radiology = ultrasound (US) may quantify degree of carotid or aortic stenosis; MRI or CT may demonstrate areas of brain ischemia; magnetic resonance angiography (MRA) or CT angiography (CTA) may locate intracranial vascular defects; echocardiography may be useful to determine if septic emboli, mural thrombus, or patent foramen ovale are cause of condition |
Treatment =
Any patient with disease attributable to atherosclerosis should be given antiplatelet (e.g., ASA) and antilipid (e.g., statins) therapy Carotid endarterectomy or angioplasty performed for carotid narrowing >60% in asymptomatic men, >50% in symptomatic men, and >70% in symptomatic women β-blockers, valvuloplasty, or valve replacement used in treatment of aortic stenosis Long-term anticoagulation used for arrhythmias Treat other underlying disorders |
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H/P =
Sudden appearance of focal neurologic deficit lasting >24 hr Constellation of symptoms depends on location of pathology Stable findings indicate stable stroke, but progressive findings indicate evolving stroke Thorough serial neurovascular examinations are important to determining region of involvement and evolution |
Stroke (cerebrovascular accident [CVA])
Acute focal neurologic deficit lasting >24 hr caused by ischemia of brain via impaired perfusion (i.e., ischemic stroke) or hemorrhage (i.e., hemorrhagic stroke) Ischemic stroke may be thrombotic (i.e., obstruction of supplying artery by clot) or embolic (i.e., blockage of supplying artery by embolization of distant thrombus) Risk factors = increased age, family history, obesity, DM, HTN, tobacco use, atrial fibrillation (Afib) Area of neurologic deficit is dependent on location of stroke Complications = better prognosis for recovery in young patients with greater overall health and limited deficits; some deficits may not improve despite treatment risk factors for stroke by the mnemonic HEADACHES: HTN, Elderly, Afib, DM, Atherosclerosis, Cardiac defect (patent foramen ovale), Hyperlipidemia, Excess weight (obesity), Smoking stroke in young patients by the 7 Cs: Cocaine, Cancer, Cardiogenic emboli, Coagulation (excessive), CNS infection (septic emboli), Congenital vascular lesion, Consanguinity (genetic disease). |
Radiology = CT without contrast or MRI useful to differentiate ischemic from hemorrhagic stroke; MRA or CTA may be helpful for locating ischemic cause
Electrocardiogram (ECG) = detection of new onset arrhythmia or history of Afib seen on prior ECG may be useful in determining cause Treatment = Acute treatment of ischemic stroke Thrombolytic therapy can be administered for ischemic stroke if within 3 hr of onset and no contraindications (i.e., evidence of hemorrhage on CT, recent surgery, anticoagulant use, recent hemorrhage, blood pressure >185/110 mm Hg) exist Antiplatelet therapy should be started within 48 hr of the event to prevent additional strokes Heparin or low molecular weight heparin (LMWH) may be considered in patients suspected of having progressive thromboembolism causing worsening symptoms Lipid-lowering drugs should be started after the acute stages of stroke in addition to optimization of blood pressure control Acute treatment of hemorrhagic stroke Reversal of anticoagulation, control of blood pressure, and control of ICP (e.g., mannitol, hyperventilation, anesthesia) Surgical decompression may be considered for collections causing decreased consciousness Antiplatelet drugs can be restarted 2 wk after stroke if patient is stable Physical therapy is useful in improving persistent functional deficits |
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Stroke
Contralateral lower extremity and trunk weakness |
Location of Stroke=ACA
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Stroke
Contralateral face and upper extremity weakness and decreased sensation, bilateral visual abnormalities, aphasia (if dominant hemisphere), neglect and inability to perform learned actions (if nondominant hemisphere) |
Location of Stroke=MCA
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Stroke
Contralateral visual abnormalities, blindness (if bilateral PCA involvement) |
Location of Stroke=PCA
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Stroke
Focal motor or sensory deficits, loss of coordination, difficulty speaking |
Location of Stroke=
Lacunar arteries |
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Stroke
Cranial nerve abnormalities, contralateral full body weakness and decreased sensation, vertigo, loss of coordination, difficulty speaking, visual abnormalities, coma |
Location of Stroke=Basilar artery
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H/P = headache, nausea, vomiting; change in mental status, focal motor or sensory deficits, possible seizure
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Parenchymal hemorrhage
Bleeding within brain parenchyma caused by HTN, arteriovenous malformation (AVM), brain aneurysm, or stimulant abuse Complications = significant supratentorial bleeding can cause transtentorial (uncal) herniation (brainstem damage) and CSF flow obstruction (leading to hydrocephalus and brainstem compression); large hemorrhages are frequently fatal |
Radiology = CT without contrast used to localize and determine extent of bleeding; MRA or CTA may be useful for locating site of bleed
Treatment = supportive care, maintain normal ICP, anticonvulsants for seizure prophylaxis; surgical decompression for large hemorrhages to reduce risk of herniation; surgical repair of AVMs or aneurysms frequently required |
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H/P = sudden severe headache, neck pain, nausea, vomiting; fever, loss of (or decreased) consciousness, possible seizure
Labs = LP shows red blood cells, xanthochromia (i.e., yellowish discoloration of CSF), increased pressure |
Subarachnoid hemorrhage (SAH)
Bleeding between the pia and arachnoid meningeal layers because of rupture of arterial aneurysm (i.e., berry aneurysm), AVM, or trauma Complications = recurrence of bleeding, arterial vasospasm, hydrocephalus; permanent neurologic damage or death may result |
Radiology = CT without contrast shows blood in the subarachnoid space; MRA or angiography can localize site of bleeding
Treatment = prevent increase in ICP (raise head of bed, administer mannitol), treat HTN, reverse anticoagulation, administer anticonvulsants, perform interventional radiologic or surgical clipping or embolization of aneurysm or AVM |
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H/P = possible initial “lucid interval” between start of bleeding and onset of symptoms for a few hours or less with no change in consciousness; severe headache, decreased consciousness, nausea; hemiparesis, hemiplegia, seizures, pupil abnormalities (i.e., “blown” pupil)
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Epidural hematoma
Collection of blood between dura and skull caused by arterial hemorrhage Complications = permanent neurologic injury or death usually results without prompt treatment |
Radiology = CT without contrast shows convex hyperdensity compressing the brain at site of injury, adjacent skull fracture may be apparent in traumatic cases
Treatment = emergent drainage of hematoma either under radiographic guidance or by surgical burr hole; stabilization of ICP and blood pressure |
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H/P =
Slowly progressive headache (days to weeks); change in mental status, contralateral hemiparesis, increased deep tendon reflexes (DTRs) Large hematomas can cause transtentorial herniation with decreased consciousness and pupil abnormalities |
Subdural hematoma
Collection of blood between the dura and arachnoid meningeal layers caused by rupture of bridging veins following trauma With mental status changes seen in an elderly patient with a history of falls, perform a workup for subdural hematoma |
Radiology = CT without contrast shows concave hyperdensity compressing the brain that does not cross midline
Treatment = surgical drainage or supportive therapy, depending on size of bleed and extent of neurologic deficits Do not perform an LP in patients with subdural hematoma because of increased risk of herniation. |
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Aphasia
Few words, difficulty producing words (nonfluent); good comprehension; face and arm hemiparesis, loss of oral coordination |
Broca's (expressive)
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Area Injured=Inferior frontal gyrus, dorsolateral frontal cortex, anterior parietal cortex
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Aphasia
Word substitutions, meaningless words, meaningless phrases (poor comprehension, “word salad”) |
Wernicke's (receptive)
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Area Injured=Posterior superior temporal gyrus, inferior parietal lobe
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Aphasia
Fluent speech, word substitutions, frequent attempts to correct words, word-finding pauses |
Conduction
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Area Injured = Supramarginal gyrus, angular gyrus
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Aphasia
Difficulty producing words, nonfluent speech, poor comprehension, limb ataxia |
Global
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Area Injured=Large infarcts of left cerebral hemisphere
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Seizure
Focal sensory (paresthesias, hallucinations) or motor (repetitive or purposeless movement) deficit; no loss of consciousness |
Simple partial
Area=Focal cortical region of brain |
EEG=Distinct focal conductive abnormality
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Seizure
Hallucinations (auditory, visual, olfactory), automatisms (repeated coordinated movement), déjà vu, impaired consciousness, postictal confusion |
Complex partial
Area=Focal region of temporal lobe |
EEG=Focal abnormalities in temporal lobe
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Seizure
Sustained contraction of extremities and back (tonic), repetitive muscle contraction and relaxation (clonic), brief contraction period followed by repetitive contraction-relaxation (tonic–clonic), brief repetitive contractions (myoclonic), or loss of tone (atonic); loss of consciousness, incontinence, significant postictal confusion, possible focal neurologic deficit lasting several days after seizure (Todd's paralysis) |
Generalized convulsive (tonic, clonic, tonic–clonic, myoclonic, atonic)
Area=Bilateral cerebral cortex |
EEG=Generalized electrical abnormalities
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Seizure
Brief (few seconds) episodes of impaired consciousness, normal muscle tone, possible eye blinking, no postictal confusion; more common in children |
Absence
Area=Bilateral cerebral cortex |
EEG=Generalized three-cycle/second spike and wave pattern
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H/P = uninterrupted seizures lasting >20 minutes (frequently several hours) without return to normal consciousness
EEG = shows prolonged abnormal electrical activity |
Status epilepticus
Repetitive or unremitting seizures without any period of regained consciousness Caused by withdrawal of anticonvulsants, alcohol withdrawal, trauma, preexisting seizure disorder, metabolic abnormalities Labs = complete blood count (CBC), glucose, electrolytes, toxicology, liver function tests (LFTs), blood urea nitrogen (BUN), and creatinine may be useful to determine underlying cause Complications = >20% mortality if not controlled promptly |
Treatment =
Maintain airway, breathing, circulation (ABCs) Intravenous (IV) benzodiazepines used to end seizure activity, phenytoin given to prevent recurrence Refractive seizure activity can be treated with phenobarbital or pentobarbital Treat underlying disorder |
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H/P = resting tremor (i.e., “pill rolling” tremor of hands), decreased or slowed voluntary movement (i.e., bradykinesia), mask-like facies, shuffling gait, involuntary acceleration of gait following initiation, “cogwheel” rigidity (i.e., increased tone of agonist and antagonist muscles), memory loss, difficulty initiating movement, postural instability
SMART: Shuffling gait, Mask-like facies, Akinesia, Rigidity (“cogwheel”), Tremor (resting). |
Parkinson's disease
Idiopathic dopamine depletion, loss of dopaminergic striated neurons in the substantia nigra, and Lewy body (eosinophilic cytoplasmic inclusions in neurons) formation leading to abnormal cholinergic input to cortex Similar syndrome may be induced by 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP, a side product in illicit opioid production) intoxication Tremor may originate in one limb, but can progress to several limbs. |
Treatment =
Dopaminergic agonists (e.g., levodopa, carbidopa, bromocriptine, amantadine), monoamine oxidase type B (MAO B) inhibitors (e.g., selegiline), anticholinergic agents (e.g., benztropine), amantadine (see Table 8-13) Deep brain electrical stimulation has emerged as a viable option in disease not responsive to medication alone |
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H/P = asymmetric Progressive weakness in face (e.g., tongue, dysphagia) and limbs with normal sensatioN, possible change in personality or impaired judgment; increase or decrease in DTRs, spasticity, positive Babinski sign, flaccid paralysis, and fasciculations seen in limbs
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Amyotrophic lateral sclerosis (ALS)
Progressive loss of UMNs and LMNs in brain and spinal cord, involving degeneration of anterior horn cells Complications = half of patients die within 3 yr of diagnosis secondary to respiratory failure Clinical diagnosis of ALS requires LMN signs in at least two extremities and UMN signs in one region. |
Labs = blood tests used to rule out other pathologies
Electromyogram (EMG) = demonstrates widespread muscular denervation and motor block Radiology = CT or MRI may be helpful to rule out neurologic lesions Treatment = riluzole may slow progression; supportive care (e.g., respiratory support, pain control) |
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H/P = progressive, rapid irregular involuntary movement of extremities (chorea), dementia (e.g., irritability, antisocial behavior), possible seizures
Characteristic signs include movement and mental dysfunction starting in middle age |
Huntington's disease
Autosomal dominant disease caused by multiple CAG repeats on chromosome 4; higher numbers of CAG repeats lead to earlier onset of disease Complications = usually fatal in <20 yr from diagnosis |
Labs = genetic analysis will detect chromosome 4 abnormality
Radiology = CT or MRI shows caudate nucleus and putamen atrophy Treatment = dopamine antagonists may improve chorea; genetic screening can be used in asymptomatic family members with proper counseling |
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H/P = progressive short-term memory loss, depression, confusion, inability to complete complex movements or tasks; severe cases have personality changes and delusions
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Alzheimer's disease
Slowly progressive dementia caused by neurofibrillary tangles, neuritic plaques, amyloid deposition, and neuronal atrophy; most common cause of dementia Risk factors = increased age, family history, Down syndrome; female > male Complications = median survival following diagnosis is 3 yr because of comorbidity |
Labs = nondiagnostic, but can be used to rule out other causes of dementia
Radiology = CT or MRI shows cortical atrophy Distinguish dementia from Alzheimer's disease from that caused by multiple cortical infarcts with MRI. Multiple small lesions or infarcts will be apparent on MRI when the cause is vascular. Treatment = cholinesterase inhibitors (e.g., donepezil, rivastigmine, galantamine) and vitamin E may slow progression; memantine may improve symptoms in moderate disease; occupational therapy helpful to prolong independence |
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H/P =
Variable initial presentation with multiple neurologic complaints (e.g., vertigo, vision abnormalities, paresthesias, weakness, urinary retention) that are difficult to explain through one cause Symptoms may progress slowly with several remissions and become worse during stressful events (e.g., infection, childbirth, trauma, heat) Late symptoms and signs include worsening vision, poor movement control, difficulty speaking (i.e., dysarthria), sensory abnormalities, postural and positional instabilities (i.e., cerebellar signs), spasticity, increased DTRs, and positive Babinski sign Women 20–40 yr of age |
Multiple sclerosis (MS)
Progressive demyelinating disease of brain and spinal cord with possible autoimmune etiology Complications = progressive neurologic abnormalities with residual deficits; many patients become chronically disabled |
Labs = LP shows CSF with increased protein, mildly increased WBCs, oligoclonal bands, increased IgG
Radiology = MRI shows multiple asymmetric white matter lesions Treatment = corticosteroids, methotrexate, and avoidance of stress may help decrease length of exacerbations; interferon-β and glatiramer acetate decrease frequency of exacerbations; supportive care for worsening neurologic dysfunction |
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H/P = symptoms and signs depend on relation of nerve roots to cavity
Local to cavity: loss of pain and temperature sensation, flaccid paralysis, decreased DTRs, fasciculations Below cavity: loss of proprioception and vibration sense, spasticity, increased DTRs |
Syringomyelia
Post-traumatic cystic degeneration of spinal cord from an unknown mechanism Syrinx cavity (i.e., centralized channel within spinal cord) expands and compresses adjacent neural tissue |
Radiology = MRI shows syrinx expansion
Treatment = surgical decompression; shunting may be needed for recurrent cases; supportive care |
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H/P = periodic weakness and muscle fatigue that worsens through day; ptosis, diplopia (i.e., double vision), dysphasia; in severe cases, patients have dyspnea
Most common in young adult women Labs = positive ACh receptor antibodies; when edrophonium is administered, symptoms improve (i.e., Tensilon test); nerve stimulation and EMG are helpful in making diagnosis |
Myasthenia gravis
Autoimmune disorder characterized by antibodies that bind to acetylcholine (ACh) receptors at neuromuscular junction and block normal neuromuscular transmission resulting in easy fatigability Often associated with thymoma and thyrotoxicosis |
Treatment = anticholinesterase agents (e.g., neostigmine, pyridostigmine), thymectomy, immunosuppressive agents (e.g., prednisone, azathioprine), plasmapheresis, IV immunoglobulin for refractive cases
If myasthenia gravis is diagnosed in a patient, always perform a chest CT to look for a thymoma. |
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H/P = periodic weakness and muscle fatigue that worsens through day; ptosis, diplopia (i.e., double vision), dysphasia; in severe cases, patients have dyspnea
Paraneoplastic disorder (e.g., small cell lung cancer) |
Lambert-Eaton syndrome
antibodies to presynaptic Ca2+ channels |
Treatment=immunosuppressive agents and plasmapheresis.
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H/P =
Rapidly progressive bilateral weakness initially in distal extremities in “stocking-glove” distribution and extending proximally, with decreased sensation and possible absent DTRs; possible severe neuropathic pain Recent history of viral infection, vaccination, or surgery Blood pressure, heart rate, or core temperature may be labile Severe cases may include respiratory muscle weakness Labs = LP shows increased protein, with normal pressure and glucose |
Guillain-Barré syndrome
Autoimmune demyelinating disorder of peripheral nerves associated with recent viral infection, surgery, or vaccination (rare) Complications = respiratory failure requires intubation and ventilation; most patients recover fully |
EMG = consistent with widespread demyelination
Treatment = self-resolving within 1 month; plasmapheresis or IV immunoglobulin may accelerate resolution; patients must be watched for signs of respiratory failure; adequate analgesia for neuropathic pain |
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/P = hypersensitive and painful limb following recovery from injury, edema, atrophy; abnormal tone and increased sweating at involved site; occasional cyanosis or increased hair growth at injury site
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Complex regional pain syndrome (CRPS) (a.k.a. reflex sympathetic dystrophy [RSD])
Chronic pain syndrome that occurs after trauma because of abnormal neurologic reorganization at site of injury (pain fibers may become “wired” into sympathetic neuronal pathways) |
Radiology = bone scan or MRI may show decreased perfusion of injured site; x-rays may show osteopenia
Treatment = Selected nerve blocks with sensation testing may help differentiate RSD from other neuropathies Physical therapy, transcutaneous electrical nerve stimulation (TENS), regional nerve block, topical anesthetics, and corticosteroids have been suggested as initial therapies Corticosteroids and anticonvulsants may be useful in refractory cases |
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Fixed oscillation of hands or head
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Benign essential tremor
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Treatment=β-blockers, primidone, clonazepam; thalamotomy or deep brain stimulation in refractory cases
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Rapid flinching distal limb and facial movements
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Chorea
association=Hyperthyroidism, stroke, Huntington's disease, SLE, levodopa use, rheumatic heart disease |
Treatment=Treat the underlying disorder
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Snake-like movement in extremities
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Athetosis
associated w/ Cerebral palsy, encephalopathy, Huntington's disease, Wilson's disease |
Treatment=Treat underlying disorder
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Slow writhing proximal limb and trunk contractions
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Dystonia
associated w/ Wilson's disease, Parkinson's disease, Huntington's disease, encephalitis, neuroleptic use (tardive dyskinesia) |
Treatment=Carbidopa, levodopa, botulinum toxin, treat underlying disorder
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Flinging of proximal extremities
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Hemiballismus
associated w/ Stroke (subthalamic nucleus) |
Treatment=Haloperidol
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Repetitive brief involuntary movement (blinking, grimacing) or sound (grunting, sniffing, throat clearing)
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Tics
associated w/ Tourette's syndrome, obsessive- compulsive disorder, attention deficit hyperactivity disorder |
Treatment=Clonidine, haloperidol, methylphenidate, dextroamphetamine
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H/P = headache, vomiting, lethargy; focal neurologic abnormalities, change in mental status, possible seizures; blown pupil seen if herniation occurs
Symptoms result from focal compression (i.e., mass effect) of tumor (e.g., hydrocephalus, increased ICP, venous obstruction) |
Primary CNS neoplasms
Brain tumors that are not caused by distant metastases; more common in young and middle-aged adults (see Table 8-15) Tumors in adults tend to be above the tentorium (i.e., fold of dural meninges that separates cerebellum below from cortex above) Tumors in children tend to be below the tentorium |
Labs = biopsy under CT guidance of detected lesion used for diagnosis
Radiology = MRI or positron emission tomography (PET) scan detects lesion Treatment = surgical resection (if possible), radiation, chemotherapy; corticosteroids may decrease cerebral edema; anticonvulsants used for seizure prophylaxis |
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H/P = symptoms similar to presentation for primary tumors; headache, vomiting, lethargy; focal neurologic abnormalities, change in mental status, seizures
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Metastatic CNS neoplasms
Tumors that have metastasized to brain from distant site; lung, breast, kidney, renal, gastrointestinal (GI) tract, melanoma are most common primary tumors Complications = poor prognosis |
Labs = biopsy confirms origin of tumor
Radiology = MRI is most-commonly used tool to detect lesions Treatment = treat original tumor; surgical resection for single metastasis, palliative radiation Full search for a source neoplasm (full body CT, blood cancer antigens |
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CNS tumor
Headache, seizures, focal neurologic deficits |
Meningioma
@ dura mater prognosis = good |
Treatment=Surgical resection, radiation
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CNS tumor
Headache, gradual increase in ICP, facial sensory and motor deficits |
Astrocytoma
@ cortex Median survival 7.5 yr |
Treatment=Surgical resection, radiation
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CNS tumor
Headache, rapid increase in ICP, sensory and motor deficits |
Glioblastoma multiforme (high-grade astrocytoma)
@ cortex Poor; median survival <1 yr |
Treatment=Surgical resection, facial radiation, chemotherapy
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CNS tumor
Headache, gradual increase in ICP, facial sensory and motor deficits |
Oligodendroglial tumor
@cortex 75% 5-yr survival if low grade |
Treatment=Surgical resection, radiation
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CNS tumor
Headache, seizures, focal neurologic deficits immuno-compromised patients |
CNS lymphoma
@ Meninges or cortex Variable; poor in HIV-positive patients |
Treatment=Corticosteroids, radiation, chemotherapy
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CNS tumor
Hydrocephalus, increased ICP |
Medulloblastoma
@ 4th cerebral ventricle poor prognosis |
Treatment=Surgical resection, radiation, chemotherapy
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H/P =
Initial signs are freckling, café-au-lait spots, Lisch nodules, neurofibromas, and bone abnormalities evident in first few years of life Severe functional limitations seen in movement and gait caused by nonunion of bone fragments (i.e., pseudoarthrosis) and fractures during development Short stature and scoliosis may be evident Visual abnormalities may result from compression of optic nerve by glioma Possible cognitive impairments, seizures, or peripheral neuropathic signs |
Neurofibromatosis type 1 (von Recklinghausen's disease)
Autosomal dominant disorder (NF1 gene on chromosome 17) with multiple neurologic tumor and dermatologic manifestations Neurofibromatosis type 2 is a rare autosomal dominant disorder linked to chromosome 22, characterized by the development of bilateral acoustic neuromas 2 of following for diagnosis: >5 café-au-lait macules >15 mm diameter >1 neurofibromas or 1 plexiform neurofibroma (i.e., tumors with mix of Schwann cells, fibroblasts, and mast cells) Axillary or inguinal freckling Optic glioma (i.e., tumor of optic nerve) >1 iris hamartomas (i.e., Lisch nodules) Bone lesions (e.g., cortical thinning of long bones, sphenoid dysplasia) First-degree relative with neurofibromatosis type 1 |
Labs = genetic testing detects abnormal gene
Radiology = MRI shows multiple areas of increased signal intensity in brain and increased brain volume Treatment = therapy directed at maintaining function and treating complications Complications = increased risk of malignant CNS tumors, developmental delays, mental retardation, peripheral neuropathy, pheochromocytoma, vision abnormalities, severe bone abnormalities, seizures |
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H/P = possible sudden loss of muscle tone (i.e., cataplexy), vivid dreams, sleep paralysis; hypersomnia (i.e., sudden occurrence of sleep) may occur suddenly during the daytime
Labs = polysomnography may show multiple arousals and decreased latency until REM sleep |
Narcolepsy
Persistent excessive daytime sleepiness regardless of prior sleep quality |
Treatment = modafinil (preferred), methylphenidate, or pemoline help prevent hypersomnia, tricyclic antidepressants may help prevent cataplexy; establishing regular sleep schedule with short naps improves wakefulness
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/P = possible prodrome of lightheadedness, nausea, and weakness preceding loss of consciousness (i.e., fainting); few generalized spasms may be observed; Patient quickly regains consciousnesS (although seizure patients may display postictal sleepiness); hypotension, arrhythmias, neurologic deficits may be detected following the episode
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Syncope
Acute transient loss of consciousness frequently related to inadequate blood supply to the brain Common causes include cardiac dysfunction (e.g., aortic stenosis, bradycardia, decreased stroke volume), vasovagal response, hypotension, hypoglycemia, seizures, cerebrovascular ischemia |
Labs = glucose levels should be measured; orthostatics or tilt testing (i.e., patient response is measured with rapid posture changes), with or without β-blocker infusion, can help diagnose cardiovascular cause; echocardiography or stress testing may be useful
ECG = useful for diagnosing cardiac causes; ambulatory monitoring may be used to measure extended periods of time EEG = useful for detecting epileptic causes Radiology = MRI, MRA, or angiography may detect vascular abnormalities Treatment = treat underlying cause |
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H/P = patient unresponsive to stimuli; pertinent history and physical examination helpful for determining cause; CN examination particularly helpful for determining level of injury
(see Figure 8-6) |
Coma
Condition in which patient is unresponsive to stimuli and unable to be aroused; associated with bilateral cortical or brainstem reticular activating system dysfunction Can result from cerebral hemorrhage, tumor, abscess, sedating drugs (e.g., alcohol, benzodiazepines, narcotics), hypoglycemia, metabolic dysfunction, hypothermia, hepatorenal failure, or psychogenic causes |
Labs = CBC, electrolytes, BUN and creatinine, glucose, LFTs, coagulation factors, toxicology, CSF analysis, EEG, or arterial blood gas are helpful for diagnosis
Radiology = CT or MRI may detect intracranial cause (e.g., hemorrhage, tumor) Treatment = maintain ABCs; prevent increase in ICP (hyperventilation, mannitol, elevate head); treat underlying cause |
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H/P = fever >102°F/38.9°C with rapid rise in temperature; tonic–clonic seizure lasting <15 minutes; atypical seizures can occur at lower temperature and last longer
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Febrile seizures
Childhood seizures between 6 months and 6 yr of age associated with fever Occur in absence of CNS infection or lesion, metabolic abnormality, or history or prior afebrile seizures Complications = 35% of patients have recurrent febrile seizures, but little increase in lifetime risk of epilepsy Atypical febrile seizures more likely to recur, occur over longer periods of time, and carry an increased risk of epilepsy |
Labs = LP should be performed if meningitis suspected or in children <12 months of age
EEG = usually normal, unless atypical seizure Treatment = confirm respiratory stability; acetaminophen as antipyretic; atypical seizures should receive more in-depth workup, including blood laboratory studies, EEG, and MRI |
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H/P = increased head growth, bulging fontanelles, and dilated scalp veins in infants; lethargy, vomiting, poor appetite, irritability, headache, diplopia, papilledema, poor skull suture fusion in older children
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Childhood hydrocephalus
Hydrocephalus in children caused by either obstruction of CSF circulation in 4th cerebral ventricle (i.e., noncommunicating) or dysfunction of subarachnoid cisterns or arachnoid villi (i.e., communicating) Complications = increased risk of epilepsy; increased risk of bacterial infection with shunting; 50% mortality before 3 yr of age if untreated Arnold-Chiari malformation type II and Dandy-Walker malformations are anatomic defects of the skull and ventricular system associated with hydrocephalus in children |
Labs = LP should be performed if infection is suspected
Radiology = US, CT, or MRI will show expanded ventricles Treatment = acetazolamide or furosemide can be used temporarily to relieve symptoms; surgical shunting usually required for most cases |
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H/P = poor development after first few months of life, decreased alertness, hyperacute hearing; cherry-red spots on retina on funduscopic examination, progressive paralysis, vision loss, change in mental status
Labs = decreased hexosaminidase A activity; DNA analysis confirms diagnosis |
Tay-Sachs disease
Autosomal recessive disorder caused by absence of hexosaminidase A (i.e., enzyme required for lipid ganglioside metabolism) Risk factors = Ashkenazi Jews, French Canadians |
Treatment = supportive care; genetic screening may aid parents with future childbearing decisions
Complications = death within first few years of life |
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H/P =
Symptom severity depends on defect severity; patients with mild spina bifida may have tuft of hair over defect and may be asymptomatic More severe cases of spina bifida can include delayed motor and mental development More severe neural tube defects have more severe neurologic and developmental abnormalities Anencephalic neonates have only brainstem function and no upper cortical function |
Neural tube disorders
Failure of neural tube closure during gestation leading to a spectrum of defects involving CNS formation Types of defects Spina bifida occulta: most benign type; defect in closure of dorsal vertebral arches above spinal cord (usually lumbosacral junction) Meningocele: larger defect with herniation of meninges through dorsal vertebral defect; soft mass may form in midline superficial to defect Myelomeningocele: severe defect with herniation of meninges and spinal cord through defect; frequent neurologic deficits, including bowel and bladder incontinence, flaccid paralysis, poor sensation, LMN signs, hydrocephalus Anencephaly: severe disorder with failure of cranial neural tube to close; absence of forebrain, meninges, and portions of skull; death occurs within days of birth Risk factors = anticonvulsant use or poor folate intake during pregnancy (both result in low maternal serum folate), DM Complications = increased risk of urinary tract infection and CNS infection; hydrocephalus in severe defects; children with severe defects may require lifelong care; survival time for anencephaly is typically for only a few days following birth |
Labs = increased amniotic α-fetoprotein and acetylcholinesterase during gestation (measured in properly timed quadruple screen)
Radiology = US during pregnancy may detect defects Treatment = Surgical repair of all but mild defects needed Shunting frequently needed for meningocele and myelomeningocele to resolve hydrocephalus Physical therapy needed for gait abnormalities for patients capable of walking (spina bifida) Fetal surgery is developing as a potential treatment for lower neural tube defects diagnosed in utero Appropriate supportive care for children with more severe neurologic deficits and those involving the genitourinary system Pregnant women and women trying to conceive should be given folate supplementation to reduce risk of defects |
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H/P =
Patients with spastic CP have multiple limbs with increased tone, increased DTRs, weakness, gait abnormalities, and frequent mental retardation P.191 Patients with dyskinetic CP have choreoathetoid, dystonic, or ataxic movements that worsen with stress as well as difficulty speaking (i.e., dysarthria) Both types of CP can include hyperactivity, seizures, or limb contractures Some patients may exhibit symptoms of both types |
Cerebral palsy (CP)
Disorders of motor function resulting from CNS damage during in utero or infantile development; most cases result from perinatal complications Risk factors = prematurity, intrauterine growth restriction, birth trauma, neonatal seizures or cerebral hemorrhage, perinatal asphyxia, multiple births, intrauterine infection Types Spastic: spastic paresis of multiple limbs Dyskinetic: choreoathetoid (see hyperkinetic disorders in this chapter), dystonic, or ataxic movement disorder Spastic CP is caused by damage of pyramidal tracts. Dyskinetic CP results from extrapyramidal pathology. |
Radiology = MRI may be useful for detecting causative lesions
Treatment = Pharmacologic therapy (e.g., botulinum toxin, dantrolene, baclofen, benzodiazepines), physical therapy, bracing, and surgery can be used to alleviate contractures and improve function Speech therapy is useful for dysarthria Special education is needed for patients with mental retardation Social and psychological support will be needed to help parents coordinate the many services needed for chronic care |
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H/P = rarely, patients experience decrease in vision or eye inflammation; ophthalmologic examination may detect poor red-light reflex in affected eye (i.e., leukocoria) or white retinal mass
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Retinoblastoma
Malignant tumor of retina in children and the most common intraocular tumor in children Some cases have a genetic link that increases risk of tumor for both eyes Complications = good prognosis if metastasis has not occurred; risk of vision loss is high if tumor is adjacent to cornea |
Labs = mutation of RB1 gene apparent on genetic testing
Radiology = US and CT detect size and extent of tumor; finding of calcified mass with normal globe size on CT is needed before therapy can be initiated Treatment = Enucleation performed for large tumors with no vision potential Radiation can be used for bilateral tumors or tumors near optic nerve Cryotherapy or laser photocoagulation used for smaller tumors Chemotherapy used for metastases or vision salvage |
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H/P = mildly painful eye, inflamed conjunctiva, possible lymphadenopathy, pruritic eye when caused by allergy; purulent discharge seen with bacterial infection
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Conjunctivitis
Inflammation of eye mucosa secondary to bacterial (e.g., Staphylococcus aureus, S. pneumoniae) or viral infection or allergic reaction |
Labs = Gram stain and culture of discharge may indicate bacterial cause
Treatment = self-limited; topical sulfonamides or erythromycin reduce duration of bacterial infection; antihistamines improve symptoms caused by allergic reaction; fastidious handwashing decreases community spread of infection |
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H/P = pain and photophobia; slit lamp examination shows inflammation of eye and keratin deposits on cornea
or H/P =mild vision abnormalities; slit lamp examination shows eye inflammation and retinal lesions |
Anterior/Posterior Uveitis
Inflammation of iris, choroids, and ciliary bodies caused by infectious (e.g., viral, syphilis), autoimmune (e.g., ankylosing spondylitis, juvenile rheumatoid arthritis), or inflammatory (e.g., ulcerative colitis, Crohn's disease) conditions |
Treatment = topical antibiotics if caused by infection; topical or systemic corticosteroids if not caused by infection; treat underlying condition
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H/P = progressive hazy and blurred vision occurring over months to years; examination reveals opacity of lenses and decreased red reflex
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Cataracts
Clouding of lens leading to progressive vision loss Risk factors = trauma (caustic substances), DM, corticosteroid use, age, low education, alcohol use, tobacco use |
Treatment = lens replacement surgery
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H/P = initially asymptomatic; gradual loss of visual fields (from Peripheral to Central), halos seen around lights, headache, and poor adaptation to changes in light; Cupping of optic disc seen on funduscopic examination
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Open angle glaucoma
Gradual bilateral increase in IOP Risk factors = increased age, increased IOP, blacks, DM, myopia, family history Complications = progressive, permanent vision loss Any patient who requires frequent changes of lens prescriptions should be suspected of having glaucoma and pressure testing should be performed. |
Labs = IOP testing (i.e., tonometry) shows increased pressure over several tests performed at 2- to 4-wk intervals
Treatment = Topical β-blockers (e.g., timolol) and α-adrenergic agonists decrease aqueous humor production; prostaglandin analogues, α-adrenergic agonists, and cholinergic agonists (e.g., pilocarpine) increases aqueous humor removal Laser surgery improves aqueous humor drainage in refractory cases Prevention is important for all at-risk patients, who should receive regular ophthalmologic examinations |
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H/P = severe eye pain, blurred vision, halos seen around lights, nausea, and vomiting; eye is inflamed and Hard with a Dilated and Nonreactive pupil
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Closed angle glaucoma
Acute increase in IOP secondary to narrowing of anterior chamber angle and obstructed drainage of aqueous humor from eye Risk factors = increased age, Asian, hyperopia, dilated pupils (e.g., low-light environments, optometry examination dilation) Complications = rapid permanent vision loss Closed angle glaucoma is usually unilateral. Never induce additional pupil dilation during examination of patient with suspected closed angle glaucoma because it will acutely worsen the condition. |
Labs = tonometry demonstrates increased IOP
Treatment = Acetazolamide decreases pressure; pilocarpine administered after pressure is lowered to reduce obstruction Laser iridotomy should be performed to prevent recurrence (frequently performed on unaffected eye as prophylaxis |
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H/P = painless, gradual loss of vision (Central to Peripheral) at all distances; retinal pigmentation (atrophic type) and hemorrhage (exudative type) in macular region and possible retinal detachment seen on funduscopic examination
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Macular degeneration
Atrophic (slow) or exudative (rapid) degeneration of retina, leading to retinal fibrosis and permanent vision loss Risk factors = white, tobacco, family history, increased age, prolonged sunlight exposure, HTN; female > male Complications = treatment effectiveness is limited; gradual progression to severe vision loss Macular degeneration is the most common cause of bilateral vision loss in the elderly. |
Radiology = fluorescein angiography may show neovascular membranes and retina
Treatment = dietary supplementation with vitamin C, vitamin E, copper, and zinc may slow progression; intravitreal ranibizumab may help treat exudative lesions near the fovea; laser photocoagulation of discrete lesions may delay progression |
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H/P = painless acute loss of vision (“window shade pulled over eye” or numerous “floaters”); pigmented fragments or gray retina floating in vitreous humor seen on funduscopic examination
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Retinal detachment
Separating of retina from adjacent epithelium, leading to acute vision loss Risk factors = trauma, cataract surgery, myopia, family history |
Treatment = laser photocoagulation or cryotherapy to halt tear progression and reattachment of retina (may not fully restore loss of vision)
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H/P = sudden painless loss of vision; funduscopic examination shows Cherry-Red spot in fovea and poor arterial filling
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Retinal artery occlusion
resulting in sudden loss of vision Most commonly caused by atherosclerosis, DM, HTN, thromboembolic disease |
Treatment =
Thrombolysis of arterial occlusion should be performed within 8 hr of onset Acetazolamide and O2 administration also used to decrease congestion and increase perfusion for arterial occlusion |
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H/P = Retinal vein occlusion: more gradual painless loss of vision; funduscopic examination shows Cotton wool spotS, edema, Retinal hemorrhageS, and dilated veins
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Retinal vein occlusion
resulting in sudden loss of vision Most commonly caused by atherosclerosis, DM, HTN, thromboembolic disease |
Treatment = Laser photocoagulation may be useful for venous occlusion
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Pupil and Gaze Abnormalities
Accommodation to near objects, nonreactive to light |
Argyll-Robertson pupil
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Cause:Syphilis, SLE, DM
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Pupil and Gaze Abnormalities
Light in affected pupil causes minimal bilateral constriction, light in normal pupil causes normal bilateral constriction |
Marcus Gunn pupil
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Cause: Afferent nerve defect
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Pupil and Gaze Abnormalities
Ptosis, miosis, anhidrosis |
Horner's syndrome
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Cause: Sympathetic trunk lesion (e.g., Pancoast tumor)
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Pupil and Gaze Abnormalities
Minimally reactive dilated pupil |
Adie's pupil
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Cause: Abnormal innervation of iris
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Pupil and Gaze Abnormalities
With lateral gaze there is absent contralateral eye adduction |
MLF syndrome
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Cause: Intracranial lesion, MS
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H/P=Blurred vision, vision quality worsens as objects move farther away
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Myopia
Refracting power of eye is too great, causing image focal point to be anterior to retina |
Treatment=Corrective lenses, laser correction
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H/P=Blurred vision, vision quality worsens as objects move closer
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Hyperopia
Refracting power of eye is insufficient, causing image focal point to be posterior to retina |
Treatment=Corrective lenses, laser correction
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H/P=Blurred vision
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Astigmatism
Asymmetric cornea surface, causing inconsistent refraction of light |
Treatment=Corrective lenses
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H/P=Gaze for each eye is in different directions, double vision, progressive blindness
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Strabismus
Deviation of eye unable to be overcome by normal motor control |
Treatment=Vision training, surgery frequently required to achieve bilateral alignment
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H/P=Poor visual acuity, spatial differentiation in affected eye
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Amblyopia (“lazy eye”)
Developmental defect in neural pathways of eye |
Treatment=Vision training, levodopa, carbidopa
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H/P = ear pain, decreased hearing; fever, bulging tympanic membrane with decreased mobility, poor light reflex; possible bloody discharge with perforation (i.e., otorrhea)
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Otitis media
Infection of middle ear caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pyogenes, or viruses Increased risk in children secondary to shorter and more horizontal ear canal than in adults, pacifier use, hypertrophic tonsillar tissue Complications = mastoiditis, meningitis, hearing loss, sigmoid sinus thrombosis, or brain abscess can occur in untreated cases |
Treatment =
Initially observation and supportive care For unresolved cases, amoxicillin for 10 days; resistant strains may require trimethoprim-sulfamethoxazole (TMP-SMX) or stronger cephalosporins Recurrent cases may require surgical placement of tympanic tubes to assist in middle ear drainage |
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H/P = painful, swollen ear with possible white discharge; ear canal is red and swollen, tenderness of pinna
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Otitis externa (“swimmer's ear”)
Infection of outer ear canal most commonly by S. aureus, Pseudomonas, or S. epidermis; frequently associated with water in ears (e.g., swimming) |
Treatment = topical polymyxin, neomycin, and hydrocortisone; oral cephalosporins or ciprofloxacin can be used for Pseudomonas infection or infection that spreads to involved skull; topical drying agents after H2O exposure to prevent recurrent infection
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H/P =
Brief, episodic vertigo that can occur with certain head movements and are accompanied by nausea and vomiting Nystagmus may be seen during episodes Dix-Hallpike maneuver (i.e., moving from sitting to supine while quickly turning head to side) induces symptoms and confirms diagnosis |
Benign paroxysmal positional vertigo (BPPV)
Vertigo (i.e., abnormal feeling of rotational movement leading to poor balance and coordination) caused by a dislodged otolith in the inner ear that interferes with semicircular canal stabilization |
Labs = normal thyroid-stimulating hormone (TSH) level rules out thyroid pathology
Radiology = CT or MRI can rule out intracranial lesion Treatment = physical maneuvers designed to free otolith from semicircular canal can alleviate recurrent episodes |
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H/P = acute vertigo lasting several hours, nausea, vomiting, decreased hearing, feeling of ear fullness, tinnitus (ringing in ears)
Labs = audiometry shows Low-frequency hearing losS |
Ménière's disease (endolymphatic hydrops)
Vertigo caused by distension of endolymphatic compartment of inner ear Complications = progressive hearing loss |
Treatment = anticholinergics, antiemetics, and antihistamines improve exacerbations; salt restriction and acetazolamide may reduce frequency of episodes; surgical decompression needed in refractory cases
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H/P = hearing loss, dizziness, tinnitus; unilateral facial palsy; decreased sensation may be seen on examination
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Acoustic neuroma (acoustic schwannoma)
Benign tumor of Schwann cells of CN VIII that can lead to hearing loss secondary to nerve compression Complications = large tumors can compress cerebellum or brainstem |
Labs = audiometry shows sensorineural hearing loss
Radiology = MRI can localize tumor Treatment = surgical excision |
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Hearing Loss
Audiometry shows preserved air conduction, but consistently low hearing threshold (negative Rinne test) |
Conductive hearing loss:
Pathology occurs along conductive pathway from outer ear to inner ear |
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Hearing Loss
Audiometry shows both impaired bone and air conduction (asymmetric Weber test, positive Rinne test) |
Sensorineural hearing loss: Pathology in neural pathways from ear to brain
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Anterior cerebral artery (ACA)
Regions of the Brain Supplied |
Medial and superior surfaces and frontal lobes
Supplied by |
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Middle cerebral artery (MCA)
Regions of the Brain Supplied |
Lateral surfaces and temporal lobes
Supplied by |
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Posterior cerebral artery (PCA)
Regions of the Brain Supplied |
Inferior surfaces and occipital lobes
Supplied by |
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Basilar artery
Regions of the Brain Supplied |
Midbrain, brainstem (pons)
Supplied by |
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Anterior inferior cerebellar artery (AICA)
Regions of the Brain Supplied |
Brainstem (pons)
Supplied by |
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Posterior inferior cerebellar artery (PICA)
Regions of the Brain Supplied |
Brainstem (medulla)
Supplied by |
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Dorsal columns
fxn location |
Two-point discrimination, sense vibration, sense proprioception
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Posterior spinal cord
1st order neuron: Enter at ipsilateral dorsal horn, ascend in fasciculus gracilis and cuneatus, synapse in nucleus gracilis and cuneatus 2nd order neuron: Decussate at medulla, ascend as medial lemniscus |
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Spinothalamic tract
fxn location |
Senses pain, senses temperature
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Anterior spinal cord
1st order neuron:Originate in dorsal root ganglion, synapse in dorsolateral tract of Lissauer 2nd order neuron:Decussate in ventral white commissure, ascend in lateral spinothalamic tract |
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Corticospinal tract
fxn location |
Voluntary movement of striated muscle
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Lateral spinal cord
1st order neuron:Descend from internal capsule and midbrain, decussate in medullary pyramids, descend in corticospinal tract, synapse in ventral horn through interneurons 2nd order neuron: Exit cord through ventral horn |
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Anterior cerebral artery (ACA)
Regions of the Brain Supplied |
Medial and superior surfaces and frontal lobes
Supplied by |
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Middle cerebral artery (MCA)
Regions of the Brain Supplied |
Lateral surfaces and temporal lobes
Supplied by |
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Posterior cerebral artery (PCA)
Regions of the Brain Supplied |
Inferior surfaces and occipital lobes
Supplied by |
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Basilar artery
Regions of the Brain Supplied |
Midbrain, brainstem (pons)
Supplied by |
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Anterior inferior cerebellar artery (AICA)
Regions of the Brain Supplied |
Brainstem (pons)
Supplied by |
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Posterior inferior cerebellar artery (PICA)
Regions of the Brain Supplied |
Brainstem (medulla)
Supplied by |
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Dorsal columns
fxn location |
Two-point discrimination, sense vibration, sense proprioception
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Posterior spinal cord
1st order neuron: Enter at ipsilateral dorsal horn, ascend in fasciculus gracilis and cuneatus, synapse in nucleus gracilis and cuneatus 2nd order neuron: Decussate at medulla, ascend as medial lemniscus |
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Spinothalamic tract
fxn location |
Senses pain, senses temperature
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Anterior spinal cord
1st order neuron:Originate in dorsal root ganglion, synapse in dorsolateral tract of Lissauer 2nd order neuron:Decussate in ventral white commissure, ascend in lateral spinothalamic tract |
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Corticospinal tract
fxn location |
Voluntary movement of striated muscle
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Lateral spinal cord
1st order neuron:Descend from internal capsule and midbrain, decussate in medullary pyramids, descend in corticospinal tract, synapse in ventral horn through interneurons 2nd order neuron: Exit cord through ventral horn |
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Nerve Olfactory (CN I)
fxn |
Sensory
Smell |
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Nerve Optic (CN II)
fxn |
Sensory
Sight |
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Nerve Oculomotor (CN III)
fxn |
Motor
Medial, superior, inferior rectus muscles; inferior oblique muscle, ciliary muscle, sphincter muscle of eye |
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Nerve Trochlear (CN IV)
fxn |
Superior oblique muscle of eye
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Nerve Trigeminal (CN V)
fxn |
Both
Sensation of face; muscles of mastication |
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Nerve Abducens (CN VI)
fxn |
Motor
Lateral rectus muscle of eye |
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Nerve Facial (CN VII)
fxn |
Both
Taste (anterior two thirds of tongue); muscles of facial expression, stapedius muscle, stylohyoid muscle, digastric muscle (posterior belly); lacrimal, submandibular, sublingual glands |
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Nerve Vestibulocochlear (CN VIII)
fxn |
Sensory
Hearing, balance |
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Nerve Glossopharyngeal (CN IX)
fxn |
Both
Taste (posterior one third of tongue), pharyngeal sensation; stylopharyngeus muscle; parotid gland |
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Nerve Vagus (CN X)
fxn |
Both
Sensation of trachea, esophagus, viscera; laryngeal, pharyngeal muscles; visceral autonomics |
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Accessory (CN XI)
fxn |
Motor
Sternocleidomastoid and trapezius muscles |
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Hypoglossal (CN XII)
fxn |
Motor
Tongue |
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