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Neuro Exam

Cranial Nerves

proximal weakness implies muscle or spinal cord, distal is everything else / spasticity implies corticospinal / cogwheel implies Parkinson’s or PD-like / paratonic (Gegenhalten, pushing against) implies metabolic, degenerative or drug effect

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  Romberg positive (vestibular or position sense, not cerebellar) when unsteady only with eyes closed and feet together (must be steady with eyes open, of course)
  
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  ataxia  cerebellum
  
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  apraxia  delayed initial step (wide-based → NPH and frontal lobe; loss of arm swing and shuffling gait → PD)
  

briskness more important than amplitude / Hoffman’s (common to have bilateral, symmetrical) / Babinski (always abnormal in adult) / increased with cerebral, brainstem and spinal cord disease (except in anterior horn such as ALS, which is rare), decreased with nerve or never root, variable with muscle and cerebellum

vibration lost first with neuropathy, myelopathy and brain stem / position sense lost first only with cerebral pathology (double simultaneous stimulation testing for extinction phenomenon most effective but not pathognomonic for cerebral disease)

rigidity, bruits

Cerebral (encephalopathy, right or left cerebral dysfunction)

aphasia/apraxia, dementia, seizures, homonymous hemianopia / sterognosis, graphesthesia, tactile localization, 2-point discrimination most often cerebral or high cervical cord

Brainstem/cerebellum

Spinal cord (myelopathy)

Spinal root (radiculopathy)

pain, localized weakness, decreased reflexes, sometimes numbness

Nerve (neuropathy)

can be small (pain, temp) or large (position, vibration) fibers / reflexes decreased

NMJ (MG, Eaton-Lambert)

Muscle (myopathy)

usually proximal and head flexion

Meningeal
Note: spinal cord lesions are infrequently vascular, neuropathies unlikely due to tumor unless paraneoplastic / non-localizing findings often misinterpreted include: hemiparesis, dysarthria, dysphagia, hemisensory loss
Neuroradiology Tools

MRI

CT

Ultrasound

Transcranial doppler

Cerebral Angiography

EEG
MRI tidbits
T1 spinal fluid is dark

tumor  dark

edema  white w/ contrast
T2 spinal fluid is white [there is no contrast with T2]
Diffusion weighted  distinguishes new from old stroke
Note: must order additional study of posterior fossa to look at cerebellum and hindbrain structures on MRI (normal MRI will not do this) / only commonly variable ventricle is occipital horn
Caution: risk of NSF in renal failure patients (see other)

CT scan

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  non-contrast brain scan is good for CVA unless 1) < 5mm lesion, < 12 hrs old, brainstem
  
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  contrast CT actually worse for evaluation of ICH because vasculature can appear like bleeding
  

Good for evaluation of carotid arteries

Gold standard

Status epilepticus vs. metabolic encephalopathy

3 spike and wave  absence seizures
Cranial Nerves
CN palsies by themselves do not indicated brainstem disease / limb ataxia is not only cerebellar disease, but also brainstem (cerebellar peduncles), severe position sense loss and cerebral disease (infrequently)

impaired dysdiadochokinesia (rapid alternating movements) implicates motor, pyramidal, extrapyramidal, cerebellar and is most often early finding of hemiparesis

Hypothalamus  C8-T2  superior cervical ganglion  sweating (one path) and Muller’s muscles (eyelids) and dilator pupillae / because pathway splits (can have Horner’s without anydrosis)

Retina  optic n.  chiasm  tract  pretectum  Edinger-Wesphal  CN III  ciliary ganglion  sphincter pupillae

Metabolic/diencephalic  2-3 mm reactive

Pretectum  5-6 mm, round, NR

Midbrain  4-5 mm, irregular, NR

Pons  pinpoint, reactive

Uncal herniation  ipsilateral, fixed dilated from CN III compression

Barbiturate overdose  4 mm, NR

Upward gaze  pretectum and posterior commisure

Downward gaze  riMLF

Pupil  afferent pupillary defect (APD)  implies optic nerve problem (symmetric APD may be

normal variation)
Visual Defects

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  Optic nerve – central scotoma, decreased visual acuity, unilateral altitudinal hemianopia
  
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  Optic chiasm – in pituitary tumor, central scotoma (one or both) precedes bitemporal hemianopia / it may be as subtle as a color problem, also use pinhole to correct acuity
  
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  Optic tract – contralateral homonymous hemianopia (often affecting macula) / incongruent VF defect (uncommon) also implies optic tract lesion
  
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  Optic radiations - homonymous hemianopia or quadrantanopsia, contralateral
  
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  Occipital - homonymous hemianopia or quadrantanopsia, contralateral / homonymous scotomata / bilateral altitudinal hemianopia / temporal crescent (monocular, contralateral and just about the only unilateral VF defect seen with occipital lesions (otherwise it’s the optic n.)
  

mostly of central origin (brainstem) vs. toxic effect

Others: direction fixed seen with CN VIII (contralateral nystagmus with rotary element identical in all directions of gaze), BPPV and congenital nystagmus
Diencephalic syndrome

Most common – hyperalert, euphoria, FTT (anorexia in children, obesity in adults)

Less common – vomit, nystagmus, optic atrophy, polyuria (less common)
Spasmus Nutans

early childhood (1^st year) / nystagmus, head nodding / complete recovery

25% of cancer patients die with intracranial mets

-protoplasmic vs. gemistocytic (may be aggressive)

compact areas (rosenthal fibers) / loose areas (eosinophilic granular bodies and stellate astrocytes)

Pleomorphic xanthroastrocytoma

Subependymal giant cell astrocytoma

Desmoplastic astrocytoma of infancy
Meningioma

meningothelial whorl / syncytial, fibrous, transitional (may have psammoma bodies)

MRI better than CT (shows tissue better and evaluates spinal canal involvement)

may accompany von Recklinghausen’s

anaplastic oligodendroglioma

myxopapillary ependymoma - occurs in cauda equina

subependymoma

colloid cyst of 3rd ventricle

gangliocytoma

ganglioglioma - plus neoplastic glial cells

central neurocytoma - in foramen of Monroe

germinoma - most frequent pineal tumor

pineocytoma

pineoblastoma
Dementia
Incidence: 1% by 60 yrs / 5% by 65 yrs / 20% by 80 yrs / 50% by 85 yrs
Ddx: 1^st Alzheimer’s (70%), 2^nd Alcoholism, 3^rd Vascular (10%)
Neurological: Alzheimer’s, Pick’s, Lewy Body, Parkinson’s, ALS, Huntington’s, CJD, NPH, MS

Drugs: analgesics, diuretics, anticholinergics, antihypertensives, psychotropic, sedative-hypnotics

Others: infectious (HIV, neurosyphilis, lyme), toxic/metabolic (hypothyroid, Wilson’s, B₁₂ deficiency, etc), intracranial tumors, paraneoplastic syndromes
Work-Up
History

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  Use of medication (analgesic, anticholinergic, psychotropic, sedative-hypnotic)
  
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  Distinguish from depression (depression usually has poor effort in answering questions whereas dementia has good effort but incorrect answers)
  
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  Reversible causes generally do not present with constellation of findings (aphasia, apraxia, aculculia, agnosia)
  
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  Hypothyroid causes depression, irritability, mental slowing
  
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  Psychiatric, myelopathic and/or neuropathic changes of B₁₂ deficiency may occur in absence of anemia; low B₁₂ levels also may have no clinical manifestations
  
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  HIV-dementia (20% of HIV patients) often shows psychomotor slowing and focal neurological signs, but dementia is rarely the sole presentation
  
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  Cerebral vasculitis presents with progressive cognitive decline or based on area of involvement
  

Mini-mental status exam

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  CBC, urinalysis, TSH, B₁₂, folate, RPR + non-contrast head CT [~10% yield]
  
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  HIV, Apo E testing (utility debated)
  
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  CSF – reserved for atypical cases
  

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  CXR
  
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  MRI if motor dysfunction (rigidity, abnormal reflexes, asymmetry) [can diagnosis some ischemic changes missed by CT]
  
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  EEG – toxic/metabolic, subclinical seizures, Creutzfeldt-Jakob