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Neuro Flashcards

1
Q

Nondominant vs dominant parietal lobe lesions

A

Most people (90% of righties and 60% of lefties) have Left hemispheric dominance for speech and language.

Construction apraxia is seen with non-dominant (Right usually) parietal lesions. Marked difficulty copying simple line drawings.

Difficulty wearing clothes with struggling as they get into coat or pants is Dressing apraxia and is seen with bilateral or nondominant (right) parietal lesions.

You will also see confusion with nondominant lesions.

Damage to the dominant (usually L) parietal lobe, esp inferiorly leads to Gerstmann Syndrome. Trouble performing arithmetic tasks (acalcula), iniabilty to name individual fingers (finger agnosia), impaired writing (agraphia) and R/L confusion (can’t tell which side is right or left)

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2
Q

Nondominant vs dominant temporal lobe lesions

A

Nondominant temporal lobe can cause visual disorders (homonymous upper quadrantanopia) and impaired perception of complex sounds (auditory agnosia)

Dominant temporal lobe has homonymous upper quadrantanopia, and almost always involves the language functions leading to aphasia. Wenicke’s aphasia (impairment in comprehension of spoken or written language). Patients have trouble expressing thoughts in a meaninful manner. Apraxia is not seen in temporal lobe lesions

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3
Q

Pseudotumor cerebri

A

Idiopathic intracranial hypertension

Arises from chonically elevated ICP. Papilledema is evident on exam and may lead to progressie optic atrophy and blindness.

Most common in obese premenopausal women, but may also be associated with endocrine disorders (hypoparathyroidism, hypothyroidism, adrenal insufficiency, Cushing) and the usage of some meds (isotretinon, all trans retinoic acid, minocycline, tetracycline, cimetidine, corticosteroids, danazol, tamoxifen, levothyroxine, lithium, nitrofurantoin)

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4
Q

Reversible causes of falls in the elderly and potential interventions

A

Vision

  • Correction of visual acuity if less than 20/60
  • Cataract removal
  • ample lighting without glare

Postural BP

  • removal of offending meds
  • modification of salt and fluid intake
  • behavioral strategies (slow change in position)
  • compression stockings

Med use

  • removal of offending meds (benzos, neuroleptics, sleep meds)
  • reduction of polypharmacy

Balance and gait (get up and go test)

  • enviornmental modifications
  • physical therapy for gait and balance training
  • assessment for assistive device
  • exercise program

Targeted cardiovascular, msk, and neuro exam

  • diagnose and trest underlying cause if identified

home hazard eval

  • enviornmental modifications (adjust poor lighting, remove loose rugs, place non-slip bathmats and rails)
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5
Q

get up and go test

A

Assesses for postural instability in the elderly

Instruct patient to stand up from an armless chair without assistance, walk a short distance, turn around and sit down again. if patient is unsteady, further eval is needed

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6
Q

Wallenberg Syndrome

A

Lateral medullary infarct (likely from intracranial vertebral artery)

Vestibulocerebellar symptoms

  • vertigo, falling to the side of the lesion
  • dfficulty sitting upright without support
  • diplopia and nystagmus (horizontal and vertical)
  • ipsilateral limb ataxia

Sensory

  • abnormal facial sensation or pain (early)
  • loss of pain and temp in ipsilateral face and contralateral trunk and limbs

Ipsilateral bulbar muscle weakness

  • dysphagia and aspiration
  • dysarthria, dysphonia, and hoarseness (ipsilateral vocal cord paralysis)

Autonomic dysfunction

  • ipsilateral Horner’s (miosis, ptosis, anhidrosis)
  • intractable hiccups
  • lack of automatic respiration (esp during sleep)
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7
Q

lesions of thalamus or cortex vs brainstem

A

Sensory loss contralateral face and body. Cortical lesions can also be specific with aphasia, neglect, or agraphesthesia

Brainstem lesions involve cranial nerves and impair sensory perception over ipsilateral face and contralateral body

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8
Q

medulla vs pontine lesion

A

Pattern of cranial nerve involvement gives it away

Lateral mid-pontine lesions affect ipsilateral trigeminal nerve, causing weakness of muscles of mastication, diminished jaw jerk reflex and impaired tactile and position sensation.

Dysphagia, hoarseness, diminished gag is more likely lateral medullary due to CN IX and X. Motor function is typically spared in lateral medullary infarcts.

Medial medullary: branch occlusion of vertebral or anterior spinal artery. Contralateral paralysis of arm and leg and tongue deviation toward the lesion. Can also see contralateral tactile and position sense loss

Medial pontine: contralateral ataxia and hemiparesis of the face, trunk, and limbs (ataxic hemiparesis).

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9
Q

Traumatic LP

A

RBC above 6000 without xanthochromia. Can also have WBCs (about 1 per 750-1000 RBCs)

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10
Q

diaphragmatic paralysis

A

Can lead to orthopnea, which can easily be confused with CHF. Most common causes of b/l diaphragmatic paralysis are neuro diseases like ALS.

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11
Q

Parkinson Disease

A

Clinical diagnosis. Bradykinesia and tremor or rigidity are essential features. However, these can have diagnostic accuracy of only 26% at initial visit.

Levodopa or dopamine agaonists (pramipexole, bromocriptine) are typically used for initial treatment of PD symptoms. Levodopa is the most effective controlling symptoms but there are concerns about long time use. There may also be limited period of response to levodopa and a higher incidence of levodopa-related dyskinesia in patients with early-onset PD.

Therefore, some people recommend favoring levodopa in patients over 65 who have severe symptoms affecting quality of life. Dopamine agonists like pramipexole can help to save levodopa for a later time when the patient’s symptoms are more severe and it might be preferred as initial treatment in patients less than 65

Entacapone (catechol-O-methyl transferase inhibitor) can extend efficacy of L-dopa

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12
Q

Erythropoiesis in B12 deficiency

A

Ineffective erythopoiesis is a well known phenomenon in patients with B12 deficiency. Defective DNA synthesis due to megaloblastic transformation of bone marrow and intramedullary hemolysis.

Intense erythroid hyperplasia occurs but erythroid cells are not matured normally and die in the marrow. Markers of hemolytic anemia (LDH, low haptoglobin, indirect hyperbili) may become evident but reticulocyte response is typically absent in these patients.

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13
Q

GBS

A

GI illness with subsequent development of severe symmetric muscle weakness and absent deep tendon reflexes

GBS usually occurs after GI (campy) or respiratory infection generates cross-reacting antibodies to peripheral nerve components. Resultant immune-mediated polyneuropathy causes:

  • symmetric muscle weakness that usually begins in the legs
  • paresthesias
  • dysautonomia (tachy, urinary retention) that may be life-threatening
  • decreased or absent deep tendon reflexes

Patients with GBS are at high risk for deveoloping rapid onset respiratory failure due to respiratory muscle weakness. Frequent measurement of vital capacity is needed. 30% require ventilation

May want EMG and LP, but check vital capacity (tital volume and neg insp force too) first

Disease modifying treatment with plasma exchange or IVIG speeds recovery and reduces need for MV. Patients with GBS received plasma exchange or IVIG if

  • nonambulatory
  • within 4 weeks of symptom onset

Those who are ambulatory and recovering dont need treatment.

Evolution

  • 2 weeks progresssive motor weakness that an lead to paralysis
  • 2-4 weeks of plateu’d symptoms
  • slow, spontaneous recovery over months

Patients with GBS tend to have impaired neuro recovery if infection was from campy, they had severe motor weakness on admission or required ventilation

IVIG/plasma reduce recovery by 50%

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14
Q

Criteria for thrombolytics in stroke

A

Inclusion

  • Ischemic stroke with measurable deficits
  • Symptoms onset less than 3-4.5 hrs before treatment initiation

Strict exclusion

  • hemorrhage or multilobar infarct involving over 33% of cerebral hemisphere on CT
  • stroke/head trauma in past 3 months
  • history of intracranial hemorrhage, neoplasm, or vascular malformation
  • recent intracranial/spinal surgery
  • active bleeding or arterial puncture in last 7d at noncompressible site
  • BP over 185/110
  • platelets less than 100 or glucose less than 50
  • anticoagulant with INR over 1.7, PT over 15, or increased active PTT

Relative exclusion

  • minor or rapidly improving neurodeficits
  • major surgery/trauma in last 14d
  • MI in last 3 months
  • GU or GI bleeding in last 21d
  • seizure at stroke onset
  • pregnancy
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15
Q

DVT in stroke patients

A

DVT/PE is a common cause of morbidity/mortality in patients with acute stroke (highest risk at 2-7d, very high in patients with hemiparesis). For hemorrhagic stroke, use compression devices for ppx. All else get subq heparin. Don’t need full anticoagulation (risk of hemorrhagic transformation of infarct)

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16
Q

BP goals in stroke

A

If you didn’t get tPA it’s 220/120

If you did get tpa it’s 185/105 for at least 24h

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17
Q

DDx of stroke in young adult

A

Cardiac

  • patent foramen ovale
  • congenital heart disease
  • arrythmia

Heme

  • heparn induced thrombocytopenia
  • inherited or acquired hypercoaguable state
  • sickle cell disease

Infectious

  • endocarditis
  • varicella zoster virus
  • menigovascular syphilis
  • bacterial meningitis
  • TB meningitis

Other

  • Inflammatory arteritis (Takayasu)
  • Cocaine, amphetamine use
  • cerebral artery dissection
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18
Q

Clinical features of MS

A

Features suggesting MS

  • Onset at age 15-50
  • optic neuritis
  • Lhermitte’s sign
  • Internuclear ophtalmoplegia
  • Uhthoff’s phenomenon (heat sensitivity)
  • Sensory symptoms (numbness and paresthesia)
  • Motor symptoms (paraparesis and spasticity)
  • Bowel/bladder dysfunction

Disease pattern

  • Relapsing remitting (most common)
  • primary progressive
  • secondary progressive
  • progressive relapsing

Diagnosis

  • T2 MRI (preferred modality) lesions disseminated in time and space (periventricular, juxtacortical, infratentorial or spinal cord)
  • Oligoclonal IgG bands on CSF

Optic neuritis: monocular visual loss accompnied by eye pain that worsens with eye movement

Transverse myelitis: upper motor neuron signs and sensory loss below the level of spinal involvement

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19
Q

Treatment of MS

A

Acute MS exacerbation

  • oral and IV corticosteroids are equally as effective
  • patients with optic neuritis should get IV though (oral has increased risk of recurrent optic neuritis). Oral staper can be considered after IV
  • Plasmaphoreis if not responsive to steroids

Chronic maintenance

  • disease modifying agents (beta interfon, glatiramer acetate) for relapsing remitting.

Treatment doesn’t really change in pregnancy (unless they’re on teriflunomide or mitoxantrone which are contraindicated in pregnancy)

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20
Q

Symptomatic treatment of common MS findings

A

Depression - SSRIs, SNRIs

Spasticity

  • PT
  • Massage
  • Baclofen

Fatigue

  • sleep hygiene, regular exercise
  • amantadine
  • stimulants (methylphenidate, modafinil)

Neuropathic pain

  • gabapentin or duloxetine

Urge urinary incontinence

  • timed voiding
  • fluid restriciton less than 2L/d
  • antiCh (oxybutynin, tolterodine)
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21
Q

Pediatric traumatic brain injury

A

High risk features age less than 2

  • AMS (fussy)
  • LOC
  • severe mechanism of injury - fall over 3ft, high impact, MVC
  • nonfrontal scalp hematoma (large (over 3cm) parietal and temporal hematomas have highest risk))
  • palpable skull fracture

High risk features age 2-18

  • AMS (somnolence, agitation)
  • LOC
  • severe mechanism of injury - fall over 5ft, high impact, MVC
  • Vomiting, severe HA
  • basilar skull fracture signs (like CSF rhinorrhea)

Mangement of high risk featurs is CT

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22
Q

Manifestations of sarcoid

A

Pulmonary

  • bilateral hilar adenopathy
  • interstitial infiltrates

Cutaneous

  • papular, nodular or plaquelike lesions
  • erythema nodosum

Ophtho

  • anterior uveitis (iridocylitis or iritis)
  • posterior uveitis
  • keratoconjunctivitis sicca

Reticuloendothelial

  • peripheral LAD
  • Hepatomegaly
  • Splenomegaly

MSK

  • acute polyarthritis (esp ankles)
  • chronic arthritis

CV

  • AV block
  • Dilated or restrictive cardiomyopathy

CNS/endocrine

  • Facial nerve palsy!!!
  • Central DI
  • HyperCa

Lofgren syndrome

  • erythema nodosum
  • hilar adenopathy
  • migratory polyarthraliga
  • fever

Screening of suspected sarcoid begins with CXR!

Biopsy whatever you can easily get to. LAD perferred. Will show noncasseating granulomas.

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23
Q

Danger signs indicating life threatening cause of headache

A

SNOOP

  • Systemic symptoms (fever) or illness (cancer)
  • Neuro signs/symptoms
  • Onset is new
  • Other associated conditions (trauma)
  • Previous headaches with change in frequency, severity or presentation

Patients with these findings should get urgent investigation, often with imaging.

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24
Q

Ataxia, weakness, and absent deep tendon reflexes after a camping trip

A

Tick paralysis

Rare, potentially life threatening disorder n Australia and western US. Neurotoxins from the tick saliva are transmitted to host over 4-7d of tick attachment.

brief prodrome of fatigue and parasthesias. Gait ataxia and ascending paralysis that develop over hours. Absent DTRs.

Next step is meticulous skin exam. Treatment is manual removal of tick. Clinical improvement is within hours. Most will completely recover without further treatment.

Note GBS develops over several days or weeks (not hours) and is often preceded by GI/URI

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25
Q

Benign Essential Tremor

A

Most common cause of postural tremor. Incidence increases with age. familial cases are auto dominant and present younger

Present in distal upper extremities and becomes much more pronounced with outstretching of arm. Also increases at the end of an activity or movement. All patients typically have no other neuro symptoms.

Presence of family history and a slight head tremor are also seen.

Normal life expectancy. No significant disability. Treatment isnt needed and should be delayed as long as possible due to need for permanent treatment. But if causing distress or interfering with tasks/work, use propranalol (BB)

Absence of a resting tremor (worsens at rest but improves with movement), rigidity, bradykinesia or gait difficulty differentiats from tremors in parkinson.

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26
Q

HA red flags and common diagnoses

A

Sudden onset, WHOML - SAH

Age 50 and up

  • mass
  • giant cell arteritis

Increased frequency or severity

  • med overuse
  • mass
  • SDH

worsened by physical activity

  • mass
  • SAH

FND, papilledema

  • mass
  • idiopathic intracranial hypertension
  • AVM

Personality changes

  • CNS infection
  • mass
  • intracerebral hemorrhage

Systemic symptoms (fever, rash)

  • encephalitis
  • meningitis
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27
Q

Lateral femoral cutaneous nerve entrapment

A

Meralgia paresethetica

Small, purely sensory nerve off the lumbar plexus. Area of decreased sensation over the anterolateral thigh without muscle weakness or DTR issues

Reassurance and Advise weight loss and to avoid tight clothes

Local steroid injection and anticonvulsants if persistent after conservative measures

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28
Q

Femoral nerve lesion

A

Anterior and anteromedial thigh paresthesia with quads muscle weakness and decreased knee jerk

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29
Q

Obturator nerve lesion

A

Sensory loss over medial thigh and weakness in leg adduction

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30
Q

Diagnostic featurs of Dementia with Lewy Bodies

A

Central (required) - Progressive cognitive decline, dementia

Core

  • Fluctuating cognition!!
  • Visual hallucinations (detailed, recurrent)
  • Spontaneous parkinsonism features
  • REM sleep behavior disorder (dream enactment)

Suggestive

  • Severe antipsychotic sensitivity
  • SPECT or PET showing low dopamine transporter uptake in basal ganglia

Supportive

  • repeated falls
  • syncope or near syncope
  • severe autonomic dysfunction
  • delusions
  • depression or anxiety

Conflicting (make DLB less likely)

  • Neuroimaging showing cerebrovascular disease
  • Parkinsonism appearing FIRST with dementia LATER

Survival time after diagnosis is 8 years. Second most common dementia

Summary: Dementia plus at least 2 of fluctuating cognition, visual hallucination, Parkinsonism, REM sleep disorder

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31
Q

Treatment for DLB

A

Cholinesterase inhibitors for cognitive impairment pluse carbidopa-levodopa for parkinsonism.

Antipsychotics may be used to treat functionally impairing visual hallucinations or delusions BUT these patients are EXTREMELY sensitive to antipsychotics and may cause severe worseing of confusion, parkinsoism or autonomic dysfunction.

Avoid first gen and risperidone. Use quetiapine at low dose if needed.

32
Q

Concussion

A

Clinical features

  • Transient neuro disturbance (dizziness, disorientation, amnesia) after mild TBI
  • No structural intracranial injury

Management

  • Remove from same day physical play
  • neuro eval
  • rest for at least 24h
  • Gradual return to nromal activity if symptoms do not worsen
    • physical: light aerobic then nonconact sports then contact sports. If worsened symptoms, 24h rest again and return to previous step
    • neurocognitive: limited screen time, school accomodations (frequent breaks, shortened days)

return to full contact in less than 1 week is not allowed

33
Q

Carpal tunnel

A

pain and numbness in wrist and palmar surface of first 3 digits associated with repetitive movements of wrist (median nerve)

Just note:

Radial nerve - the great extensor nerve - sensory stuff on dorsal forearm and hand

Ulnar - 4-5th digits

median nerve at two heads of pronator teres - pain in volar forearm plus carpal tunnel symptoms

34
Q

Carotid endarterectomy

A

Patients with symptomatic carotid artery disease (TIA or nondisabling stroke in vascular disribution of diseased artery) who have high grade (70-99%) stenosis and a life expectancy of at least 5 years

Risks outweigh benefits in patients who are poor surgical candidates (multiple comorbidites), those with an ipsilateral stroke with persistent diabling neuro deficits and those with 100% occlusion.

All patients with atherosclerotic disease get statin, aspirin, should stop smoking and manage HTN/DM

35
Q

Clinical features of hypothyroidism

A

Generalized slowing of metabolic processes

  • weakness and fatigue
  • weight gain
  • bradycardia
  • delayed DTRs
  • constipation
  • cognitive slowing
  • cold intolerance

Matrix glycosaminoglucan accumulation

  • coarse, dry skin
  • hoarseness
  • nonpitting edema (myxedema)
  • macroglossia

Other mechanism

  • depression
  • myalgia and arthralgia
  • hypercholesterolemia

thyroid also causes hypoNa and macrocytosis

36
Q

Juvenile myoclonic epilepsy

A

Clinical

  • adolescents
  • absence seizures
  • morning myoclonus
  • generalized tonic-clonic

Diagnosis - EEG with bilateral polyspkes and slow wave activity

Management

  • valproic acid
  • avoid triggers (alcohol, sleep deprivation)

Classic is myoclonic jerks of arms in the morning in a teen aggravated by sleep deprivation and booze. GTC seizures occur later in the disease in almost all patients. Half also have a psych diagnosis like anxiety

37
Q

Infantile spasms

A

Epileptic disorder of infancy characterized by symmetric spasms, development delay and hypsarrhtymia on EEG

Corticotropin (ACTH) and vigabatrin are gold standard treatments

38
Q

NPH

A

Classic triad of gait disturbance followed by impaired cognition and urinary incontinence.

Gait is wide based and can be described as being magnetic. Cognitive impairment follows gait issues and can include early psychomotor slowing and problems with executive functioning. Urinary incontinence is last usually and should raise susipicion in someone who is already being treated for BPH.

CT has ventriculomegaly

Treat with lumbar drainage of CSF. Test functions before and after drainage. If improvement they have a high probability of responsing to definitive treatment of VP shunt

39
Q

Features of tabes dorsalis

A

Epi

  • Increased incidence of syphilis in men who have sex with men and HIV patients
  • HIV patients develop neurosyphilis more rapidly

Path

  • Trep pallidum directy damages dorsal sensory roots
  • Secondary degeneration of dorsal columns

Clinical findings

  • sensory ataxia
  • lancinating pains
  • neurogenic urinary incontinence
  • associated with Argyll Robertson pupils
40
Q

Main headache types

A

Migraine

  • Mostly female
  • often family history
  • variable onset
  • often unilateral
  • pulsatile and throbbing
  • 4-72h duration
  • associated with aura, photophobia, phonophobia and nausea

Cluster

  • mostly men
  • no FHx
  • onset during sleep
  • location often behind one eye
  • excruciating, sharp and steady
  • 15-90 min duration
  • Associated with sweating, facial flushing, nasal congestion, lacrimation and pupilary changes

Tension

  • mostly women
  • onset during stress
  • band like around the head/bilateral
  • dull, tight and persistent
  • 30min - 7d duration
  • associated with muscle tenderness in head,neck, or shoulders. Can occasionally have photophobia or phonophobia
41
Q

Nerve injury during CEA

A

Hypogloassal causes tongue deviation to site of injury.

Recurrent larygneal nerve leads to unilateral vocal cord paralysis with resultant change in voice quality

Facial nerve leads to asymmetric smile

Vagus may be injured too

Ansa hypoglossus nerve doesnt matter. Kill it at will.

42
Q

Indications for head CT after minor trauma

A

High risk patients

  • Age 65 and up
  • coagulopathy
  • drug or alcohol intox
  • high risk injury mechanism
    • pedestrian struck by car
    • ejection from vehicle
    • fall from height

High risk symptoms

  • retrograde amnesia (at least 30 mins before injury)
  • vomiting
  • seizure
  • severe HA

High risk signs

  • Glasgow 14 or less
  • suspicion of depressed skull fracture
  • signs of basilar skull fracture
    • battle sign (mastoid ecchymosis)
    • racoon eyes (orbital ecchymoses)
    • CSF rhinorrhea or otorrhea
    • hemotympanum
  • AMS or LOC
  • Neuro deficit
43
Q

Myasthenia Gravis

A

Disease of the neuromuscular junction

Classic is fluctuating muscle weakness that worsens throughout the course of the day. Most patients first notice double vision and ptosis that worsens at the end of the day which is caused by weakness in EOMs.

Next most common muscles involved are the bulbar muscles resulting in dysphagia and dysarthria

Proximal limb weakness is found less often.

Fatiguability of muscle function is key to distinguishing it from other disorders.

Autoimmune against acetylcholine receptor. There is an association between MG and thymoma.

44
Q

Wernicke encephalopathy

A

Life threatening disorder of thiamine deficiency seen most often in patients with heavy alcohol use or severe malnutrition

Classically you see

  • encephalopathy - disorientation and confusion
  • oculomotor dysfunction - lateral rectus palsy
  • gait ataxia - wide based or complete gait impairment

Give IV thiamine. All 3 symptoms are onl seen in 10% so IV thiamine has a low threshold. IF you suspect just give it.

Korsakoff syndrome is late complication of repeated or prolonged WE. Will see retrograde and anterograde amnesia often with confabulation.

Ptins with KS will have mammillary body atrophy on MRI. Patients often require long term care.

45
Q

ALS

A

Most common form of progressive motor neuron disease. Involves lower (anterior horn cells in spinal cord and brainstem neurons innervating bulbar muscles) and upper (corticospinal) motor neurons.

At onset, may involev selective loss of function of only upper or lower motor neurons but will ultimately take both

Initial sign of disease with lower motor neuron involvement is an insidiously developing asymmetric weakness, usually first evident distally in one of the limbs. Weakness is associated with progressive wasting, atrophy of muscles, and spontaneosu twitching/fasciculations of motor units. Invovlement of bulbar muscles leads to chewing/swallowing issues.

ALS with prominent corticospinal involvement has hyperactivity of muscle stretch reflexes and frequent spastic resistance to passive movements of affected limbs. Ocular motility, sensory, bowel, bladder, and cognitive functions are preserved throughout the disease.

Riluzole is a glutamate inhibitor that may prlong survival and delay need for trach

46
Q

Clinical features of opioid withdrawal

A

Presentation

  • Acute opioid cessation/dose reduction after prolonged use
  • GI - n/v, diarrhea, cramping, increased bowel sounds
  • CV - increased pulse, increased BP, sweating
  • psych - insomnia, yawning, dysphoric mood
  • other - myalgias, arthralgias, lacrimation, rhinorrhea, piloerection, mydriasis

Management

  • Opioid agonist - methadone (preferred) or buprenorphine (may worsen withdrawal bc it’s a partial antagonist)
  • Nonopioid - clonidine or adjunctive meds (antiemetics, antidiarrheals, benzo)

Opioid agonist therapy needs high levels of regulation in a supervised program. If you have a patient who just wants to leave and is unwilling to enter a supervised program choose clonidine

47
Q

Dementia subtypes

A

Alzheimer

  • Early, insidious short term memory loss
  • language deficits and spatial disorientation
  • later personality changes

Vascular

  • stepwise decline
  • early executive dysfunction
  • cerebral infarction and/or deep white matter changes on imaging

Frontotemporla dementia

  • early personality changes
  • apathy, disinhibition and compulsive behavior
  • frontotemproal atrophy on imaging

DLB

  • visual hallucinations
  • spontaneous parkinsonism
  • fluctuating cognition
48
Q

Narcolepsy

A

Recurrent lapses into sleep or napping multiple times within the same day, occuring at least 3 times weekly for 3 months

At least 1 of the following

  • Cataplexy, defined as either
    • conscious, brief episodes of sudden b/l muscle tone loss precipitated by emotions such as laughter or joking
    • spontaneous abnormal facial movements without emotional triggers
  • hypocretin-1 deficiency by CSF analysis
  • rapid eye movement sleep latency less than 15 mins

Look out for hypogogic hallucinations, fragmented sleep, excessive daytime sleepiness.

Dx with sleep study

Note: most likely cause of excessive daytime sleepiness is just not enough sleep. Consider narcolepsy only when other shit is present.

Tx: Modafinil and sleep hygiene/scheduled naps.

For cataplexy, treat with SNRIs (venlafaxine). Can also use SSRIs, TCAs, or lastly sodium oxybate.

49
Q

Amaurosis fugax

A

Sudden, transient monocular blindness.

Acute ischemic event involving the retinal artery. Condition is sudden and usually reversible. It is a marker for carotid artery atherosclerotic disease. A carotid bruit on auscultation of the next is often seen indicating significant carotid obstruction

carotid doppler eval is necessary to evaluate exten of disease and assess for need for CEA

50
Q

Bell’s Palsy

A

Rapid onset of unilateral upper AND lower facial weakness. It’s an idiopathuc neuropathy of CN 7.

Affected side will have inability to raise eyebrow or close the eye, drooping of mouth, and disappearance of nasolabial fold. Patients feel a funny feeling.

Have patient raise their eyebrows and look for symmetry. If the forehead muscles are spared, that is suggestive of intracranial lesion and should lead to imaging to evaluate for stroke/tumor.

No further workup is needed for Bell’s unless there is bilateral facial palsy, lives or has traveled to Lyme endemic area, or has other concerning features.

If there is history of travel to northeast or michigan, erythema migrans, or bilateral facial palsy get serum enzyme linked assay for Lyme.

Corticosteroids are treatment of choice. Start within 3 days to improve chance at complete recovery. Artifical tears and eye patching should be presribed. Most patients should recover within 1-6 months.

Reactivation of herpes causes most cases, but no need to treat for herpes.

Bilateral facial palsy can also occur in sarcoid. If patient had cough, SOB, CP… get CXR

51
Q

Abusive head trauma

A

Etiology

  • Blunt force to the head
  • repeated episodes of shaking

Risk

  • Child less than 1
  • young/single parents
  • unstable home enviornment

Clinical

  • SDH
  • Retinal hemorrhage
  • diffuse brain injury

Eval - emergency CT head

52
Q

Childhood absence epilepsy

A

Clinical

  • sudden impairment of consciousness (staring spells)
  • Preserved muscle tone
  • unresponsive to stimulation
  • short duration (less than 20s)
  • simple automatisms frequent
  • provoked by hyperventilation
  • many episodes per day

Diagnosis

  • EEG with 3Hz spike and wave discharges

Comorbidities

  • ADHD
  • Anxiety
  • Depression

Treatment - ethosuximide

Carbamazepine will make it worse. Others are ineffective.

Often spontaneously remits by early puberty. When patient has been seizure free for 2 years, taper the meds.

53
Q

Spina bifida

A

Path - failure of neural tube to close

Risk factors

  • prenatal maternal folate deficiency (inadequate supplementation, antifolate drugs like methotrexate)

Clinial features and comorbidities

  • motor/sensory dysfunction
  • neurogenic bladder/bowel
  • hydrocephalus
  • scoliosis

Treatent

  • surgical closure (will often cause hydrocephalus and need VP shunt)
  • clean intermittent cath
  • scheduled lax/enemas
  • bracing: correction of deformities
54
Q

Initial workup of suspected cognitive impairment

A

Cognitive Testing

  • MMSE (score less than 24 is MCI/dementia)
  • Montreal Cognitive (score less than 26)
  • Mini-Cog (abnormal 3 word recall and/or clock drawing test)

Lab testing

  • Routine - CBC, B12, TSH, CMP
  • Selective (specific risk factors) - folate, syphilis, vitamin D
  • Atypical (early onset) - CSF

Imaging

  • Routine - CT or MR
  • Atypical - EEG
55
Q

Febrile seizure

A

Risk factors

  • fever (typically with viral illness)
  • family history of seizures

Diagnostic criteria

  • Age 6 months to 5 years
  • no previous afebrile seizures
  • no signs of CNS infection
  • no acute metabolic cause (hypoglycemia)

Management

  • abortive therapy (if at least 5 mins)
  • symptomatic care (antipyretics)
  • reasurrance

Prognosis

  • no long term sequelae
  • increased risk of subsequent febrile seizure
  • slight increased risk of epilepsy (1%)
56
Q

Intravenous mannitol

A

Osmotic duretic which reduces brain volume by drawing water out of cells. It can be used to acutely lower elevated ICP in emergent situations

57
Q

Hyperventilation

A

Lowering PaCO2 by hyperventilation a patient causes cerebral vasoconstriction which lowers cerebral blood flow and reduced ICP. Hyperventilation is therefore used to decrease the PaCO2 to 25-30 mmHg and to rapidly lower ICP in emergent situations.

It is contraindicated in patients with traumatic brain injury and in acute stroke. A significant decrease in cerebral blood flow by vasoconstriction in these scenarious may lead to worsening neurological injury

58
Q

Patient with recent history of non-Hodgkin Lymphoma with classic thoracic radicular pain accompanied by weakness and sensory changes of lower extremities

A

Worry about epidural spinal cord compression

Bowel/bladder dysfunction usually develops later in course, but may be earlier in patients with compression at the level of conus.

Cancers that commonly metastasize to spine are prostate, breast, lung, nHL, RCC

It’s a medical emergency. Give high dose steroids (dexamethasone) immediately to decrease edema and pursue MRI

59
Q

Prion disease

A

Behavioral changes

Rapid progression

Myoclonus and/or seizures

60
Q

Huntington Disease

A

Auto dominant disorder that usually presents around age 40 with chorea, psychiatric symptoms (depression, anxiety), and abnormal eye movements (abnormal saccades). Symptoms of dementia typically begin later in the course.

61
Q

Brainstem glioma

A

presents with signs/symptoms of progressive brainstem involvement, including ataxia, cranial nerve palsies, and motor and/or sensory abnormalities

62
Q

PICA aneurysm

A

ataxia and bulbar stuff

63
Q

PCOM aneurysm

A

CN3 palsy (ptosis and anisocoria)

Makes up 20% of aneurysms

64
Q

Cerebral palsy

A

Risk factors

  • prematurity
  • low birth weight

Clinical

  • delayed motor milestones
  • abnormal tone, hyperreflexia
  • comorbid seizures, intellectual disability

diagnosis

  • clinical (usually by age 1-2)
  • brain MR (periventricular leukomalacia, basal ganglia lesions)

Management

  • physical, occupational and speech therapy
  • nutritional support
  • antispastic meds

Spastic is most common subtype

Early signs include delayed disappearance of neonatal reflexes (tonic neck reflex), persistent or asymmetric fisting, and early hand preference (before age 1). Hypertonia develops a few months after birth and can result in contractures and scissoring of the legs. Hyperreflexia and sustained clonus are often present.

delayed motor milestones. it’s an upper motor neuron disorder.

65
Q

Pineal gland tumor

A

Causes Parinaud’s Syndrome - loss of pupillary reaction, vertical gaze paralysis, loss of optokinetic nystagmus, and ataxia

HA is a prominent feature and is due to obstructive hydrocephalus

Some pineal tumors are germinomas and secrete HCG which can cause precocious puberty

66
Q

craniopharyngeoma

A

Classically associated with DI and a deficiency of one or more anterior pit hormones

67
Q

Major side effect of carbamazepine

A

Bone marrow suppression and neutropenia, aplastic anemia, thrombocytopenia

Elderly patients are also at risk of SIADH

Mild antiCh effects too so risk of glaucoma, urinary retention, constipation

68
Q

psychogenic coma

A

Normal response to caloric stimulation

Irrigation of external auditory canal with cold water. Normal response is a transient, conjugate, slow deviation of gase to side of the stimulus (brainstem mediated) followed by saccadic correction to the midline (cortical correction). This cannot be voluntarily suppressed. So normal oculovestibular reaction strongly suggests psychogenic coma

69
Q

phenytoin toxicity

A

earliest sign is presence of nystagmus on far lateral gaze. Some other stuff is blurred vision, diplopia, ataxia, slurred speech, dizziness, drowsiness, lethargy, and decreased mentation which can progress to coma

First step in management of side effects/high normal level is to reduce the dose (this applies to all AEDs) or alter treatment schedule.

Do not abruptly stop AEDs (taper gradually)

70
Q

transverse myelitis vs GBS

A

TM

  • motor
    • early flaccid, late spastic paralysis
    • if quadriplegia, weakness in upper is equal to lower extremities
  • sensory
    • clearly identifiable sensory level
  • autonomic
    • bowel and bladder dysfunction
  • CN’s
    • none
  • EMG/nerve conduction velocity
    • mostly normal
  • MRI
    • focal enhanced area of T2 signal
  • CSF
    • pleocytosis
    • increased IgG index maybe

GBS

  • Motor
    • ascending paralysis
    • weakness in lower is greater than upper early on
  • sensory
    • mild sensory loss
    • no spinal cord level
  • autonomic
    • cardiovascular instability
  • CN’s
    • occulomotor, glossopharnygeal, or facial paralysis
  • EMG/nerve conduction velocity
    • peripheral motor and/or sensory NCV reduced
  • MRI
    • normal
    • enhancement of anterior nerve roots or cauda equina
  • CSF
    • absence of pleocytosis
    • elevated protein
71
Q

Tuberous sclerosis complex

A

Pathophys

  • mutation (inherited or de novo) in TSC1 or TSC2
  • autosomal dominant

Clinical

  • Derm
    • ash leaf spots
    • angiofibromas of the malar region
    • shagreen patches
  • Neuro
    • CNS lesions (subependymal tumors)
    • Epilepsy (infantile spasms)
    • Intellectal disability
    • autism and behavioral disorders (hyperactivity)
  • CV
    • rhabdomyomas
  • Renal
    • AMLs

Surveillance

  • Tumor screening
    • regular skin and eye exams
    • serial MRI of brain and kindey
    • Baseline Echo and serial ECG
  • Baseline EEG
  • Neuropsych screening

If present with seizure, EEG takes priority

Most common cause of death is neuro impairment (epilepsy). Renal is number 2.

72
Q

carotid artery dissection

A

Etiology

  • Trauma: spontaneous occurence
  • underlying contributors: HTN, Smoking, Connective tissue disease

Clinical

  • unilateral head and neck pain, transient vision loss
  • ipsilateral partial Horner
    • ptosis and miosis without anhidrosis
  • signs of cerebral ischemia (focal weakness)

Diagnosis

  • CTA/MRA

Treatment

  • Thrombolysis (if within 4.5 hrs of symptom onset)
  • Antiplately therapy (aspirin) plus/minus anticoagulation

If CTA/MRA is negative but you still suspect, catheter angio is the gold standard

73
Q

STOP-Bang Survey for OSA

A

1 point for each. 0-2 is low risk. 3-4 intermediate. 4 and up is high.

Snoring

Tiredness (excessive daytime tiredness)

Observed apneas or choking/gasping

Pressure (HTN)

BMI over 35

Age over 50

Neck size (men over 17, women 16)

Gender (men)

Get a sleep study if concern

74
Q

diabetic neuropathy

A

stocking and glove pattern (symmetric distal polyneuropathy)

Look for history of ED or loss of a reflex (like cremasteric) without loss of motor function in that area.

75
Q

blepharospasm

A

Form of local dystonia. periodic involuntary eye closure that can be provoked by external stimuli (bright light or irritants) is typical.

Older women are prone to it.

Botulinum toxin injections are mainstay of treatment. Can be used for many years without losing efficacy or side effects.

76
Q

Most important modifiable risk factor for stroke

A

HTN!!!

Other ones are HLD, DM, Smoking (but HTN is king)

77
Q

Spinal epidural abscess

A

Risk factors

  • IVDU
  • immunocompromised state (DM, HIV, alcoholism)
  • infectious spread from contiguous/distant source
  • spinal trauma or surgery

Clinical features

  • classic triad: fever, severe focal back pain and neuro deficits
  • progressive symptoms: Radiculopathy, motor, and sensory deficits, bowel/bladder dysfunction and eventual paralysis

Management

  • CBC
  • Inflammatory markers (ESR/CRP)
  • Blood culture
  • MRI of spine!!!
  • CT guided aspiration/biopsy
  • empiric antibiotics
  • surgical decompression

staph aureus is 60% of infections

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