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Neuro Flashcards

1
Q

Dominant hemisphere malfunction symptoms

A

Aphasia

Alexia

Agraphia

Acalculia

Left-right disorientation

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2
Q

Non-dominant hemisphere malfunction

A

Hemineglect

Dysprosody (pseudo-foreign accent syndrome)

Amusia (inability to recognize or reproduce musical tones)

Constructional apraxia

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3
Q

Cortical vs subcortical (internal capsule) paresis

A

Cortical: different effect on face and arm vs legs

Subcortical: equal face, arm, leg involvement. Contralateral dysmetria, clumsiness. W/O sensory/cortical deficit

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4
Q

Thalamus defect

A

Contralateral dense sensory loss, severe pain

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5
Q

Subcortical structures

A

Internal capsule
Thalamus
Basal ganglia

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6
Q

Brainstem malfunction

A

Crossed hemiplagia or sensory loss:
Ipsilateral face, contralateral body

Ipsilateral cerebellar

Nystagmus toward lesion

INO

Dysphagia

Dysarthria

Hearing loss

Vertigo

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7
Q

Scanning speech

A

Cerebellum dysfunction

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8
Q

Ocular problems in cerebellum dysfunction

A

Nystagmus
Oscillopsia
Distorted smooth persuit

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9
Q

UMN vs LMN in spinal cord lesions

A

LMN at the level of lesion

UMN below the level of lesion

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10
Q

Frontal lobe testing

A

Go/no-go test

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11
Q

Ammonia smelling tests which CN?

A

V

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12
Q

Pronator drift

A

Shows contralateral UMN lesion

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13
Q

Efferent limb of pupillary light response via CN ?

A

III

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14
Q

CN palsy causing defect in sacadic eye movement

A

III

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15
Q

In CN IV palsy, head tilts toward

A

Unaffected side

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16
Q

CN V motor function

A

Temporalis, masseter, pterygoid, jaw reflex

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17
Q

UMN vs LMN facial motor lesion

A

UMN: contralateral facial weakness, sparing the brow bilaterally

LMN: ipsilateral facial weakness

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18
Q

CN IX function

A

Vocal cord function

Gag

Taste of posterior 1/3 if tongue

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19
Q

CN X

A

Vocal cord

Gag

Uvula deviation and palatal deviation

Swallowing

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20
Q

Pyramidal pattern of weakness

A

Hemiparetic gait

In upper extremity, flexors stronger than extensors. In lower extremity, extensors stronger than flexors

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21
Q

Caloric test response

A

COWS

Cold Opposite

Warm Same

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22
Q

Pattern of weakness in ALS

A

Segmental

Asymmetrical

Distal to proximal

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23
Q

DTR in motor neuron disease (ALS)

A

Increased

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24
Q

DTR in neuromuscular junction disorders

A

Normal

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25
Q

Neuromuscular disorders with fasciculation

A

Motor neuron disease (ALS…)

Peripheral neuropathy

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26
Q

DTR in myopathies

A

Normal until late

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27
Q

Neuromuscular disorder with abnormal NCS

A

Peripheral neuropathy

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28
Q

Neuromuscular disorder with autonomic symptoms

A

Peripheral neuropathy

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29
Q

Neuromuscular disorder with sensory symptoms

A

Peripheral neuropathy

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30
Q

Autonomic symptoms

A

Orthostatic hypotension

Anhidrosis

Visual blurring

Urinary hesitancy/incontinence

Constipation

Erectile dysfunction

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31
Q

Upper motor neuron tests

A

Babinski

Hoffmann

Pronator drift

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32
Q

Primitive reflexes

A

Grasp

Rooting

Palmomental

Glabellar tap

Snout

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33
Q

Thenar muscles, nerve

A

Flexor pollicis brevis

Abductor pollicis brevis

Opponens pollicis

Nerve: median (C8-T1)

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34
Q

Wasting in first dorsal webbed space

A

First dorsal interosseus muscle

Nerve: ulna

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35
Q

Interpretation of rapid alternating movement problems

A

If slow: weakness

If uncoordinated: cerebellar disorder

If slow with fatiguing and decreased amplitude: Parkinsonism

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36
Q

Cortical sensation functions exams

A

Graphesthesia

Streognosis

Extinction

2point discreminatiin

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37
Q

Coordination axams

A

Finger to nose

Heel to shin

Rapid alternating movements

Knee taps

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38
Q

Tests for stance and gait

A

Romberg

Pull test

Push and release

Gait

Tandem

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39
Q

Contraindications for LP

A

If suspect mass lesion

Infection over site

Suspect epidural abscess

Plt < 50,000

Tx with anticoagulation (high INR/PTT)

Uncooperative pt

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40
Q

Px and Tx of post-LP headache

A

Onset within 24 h
Worse when upright
Px
Smaller gauge needle

Reinsert stylet prior to needle removal

Blunt-ended needle

Tx:
Symptomatic: caffeine, sodium benzoate injection

Corrective: blood patch (autologus)

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41
Q

LP tubes

A

1: cell count

#3: smear, culture, gram stain
\+/- PCR, acid fast, bacteria Ag, fungal Ag/culture
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42
Q

Xanthochromia of CSF

A

Recent blood: SAH

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43
Q

CSF protein

A

Nl < 0.45 g/L

Viral: 0.45-1 g/L

Bacterial: > 1 g/L

Granulomatous infection: increased, but < 5 g/L (TB, fungal)

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44
Q

SCF glucose

A

Normal:
60% of serum glucose
Or
> 3.0 mmol/L

Viral: normal

Bacterial:
<25% serum
Or
<2

TB/Fungal:
Decreased. < 2-4

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45
Q

CSF cells

A

Normal:
0-5,(000,000)/ L

Viral:
<1000,(000,000)/L, lymphocytes

Bacterial > 1000, PMN

TB, fungal <1000, Lymphocytes

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46
Q

Investigations for numbness/altered sensation

A 
NCS
glucose
B12
Imaging
HIV
Lyme
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47
Q

Visual loss gait

A

Broad based

Tentative steps

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48
Q

Proprioceptive loss gait

A

Wide-based
High stepping posture
Positive Romberg

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49
Q

Periphral vestibular lesion gait

A

Vestibular ataxia

Disequilibrium

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50
Q

Peripheral nerve disorder gait

A

Steppage gait

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51
Q

Myopathic gait

A

Waddling: broad based, short stepped, pronounced lumbar lordosis, rotation of pelvis

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52
Q

Pyramidal/corticospinal gait

A

Spastic gait:
Circumduction
Scissoring

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53
Q

Basal ganglia gait

A

Parkinsonian gait:
Small paces
Stooped posture
Reduced armswing

Choreic/hemicallistic/dystonic gait

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54
Q

Cerebellar gait

A

Wide based without high stepping. Veering to side of lesion

Alcohol
Hypothyroidism
Vit E deficiency
Hypoglycemia
Hypoxia
Paraneo
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55
Q

Factors damaging olfactory neuroepithelium

A

Influenza

HSV

IFN

Leprosy

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56
Q

Eye in CN III paresy

A

Resting down and out

Ptosis

Mydriasis

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57
Q

CN III palsy symptoms due to midbrain lesion

A

Complete unilateral CN III palsy

Bilateral weakness of superior rectus and ptosis

Contralateral pyramidal signs

+/- mydriasis

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58
Q

CN III palsy with reactive pupil (pupil sparing)

A

Vascular event

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59
Q

CN III palsy with mydriasis

A

Compressive lesions

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60
Q

CN nerves damaged in cavernous sinus involvement

A

CN III
CN IV
CN V1, V2
CN VI

+ orbital pain and proptosis

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61
Q

Nerve at risk of trauma during surgery involving midbrain

A

CN IV

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62
Q

The only CN decussating at midline

A

CN IV

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63
Q

Jaw deviation in CN V palsy

A

Toward lesion

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64
Q

Head tilt in CN III palsy

A

Up and rotated away

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65
Q

Head tilt in CN IV palsy

A

Down and flexed away

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66
Q

Head tilt in CN VI palsy

A

Rotated towards

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67
Q

Viruses implicated in Bell’s palsy

A

HSV&raquo_space;> CMV, EBV, VZV

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68
Q

CN with longest intracranial course

A

CN VI

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69
Q

Screening for dysphagia

A

Pt drinks water,

Observe: cough, choking, wetness of voice

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70
Q

CN XI palsy. UMN vs LMN

A

UMN: ipsilateral SCM, contralateral trapezius

LMN: ipsilateral SCM and trapezius

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71
Q

CN XII palsy. UMN vs LMN

A

UMN: tongue deviation away from lesion. No atrophy. No fasciculation

LMN: tongue deviates towards lesion. Atrophy. Fasciculation

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72
Q

Uvula deviation in LMN CN X palsy

A

Away from lesion

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73
Q

Glossopharyngeal neuralgia Tx

A

Carbamazepine

Surgical ablation

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74
Q

Vision loss in optic neuritis

A

Rapidly progressive

Monocular

Central vision (acuity/color) loss with recovery

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75
Q

Etiologies of optic neyritis

A

Viral

MS

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76
Q

Inv for optic neuritis

A

MRI with gado

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77
Q

Fundus in optic neuritis

A

Disc swelling if anterior

Normal if retrobulbar

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78
Q

Vision in papilledema

A

Late visual loss

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79
Q

Fundus in papilledema

A

Bilateral swelling

Retinal hemorrhage

No venous pulsation

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80
Q

Inv for papilledema

A

Emergent CT

If normal CT: LP for opening pressure

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81
Q

Pain in optic neuritis

A

Painful esp with eye movement

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82
Q

Pain in AION

A

Not painful

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83
Q

Fundus in AION

A

Pale segmental disc edema

Retinal dot

Flame hemorrhages

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84
Q

Etiologies of AION

A

GCA

atherosclerosis

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85
Q

Inv for AION

A

CBC
ESR, CRP
Temporal artery Bx

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86
Q

Pain in CRVO

A

No pain

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87
Q

Vision loss in AION

A

Painless

Unilateral

Acute

Field defect

Hours to days

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88
Q

Vision loss in CRVO

A

Painless

Unilateral

Variable

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89
Q

Fundus in CRVO

A

Swollen disc

Venous engorgement

Retinal hemorrhage

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90
Q

Inv in CRVO

A

Fluorscein angiogram

Coherence tomography

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91
Q

Drug causing non-arteritic anterior ischemic optic neuropathy

A

Sildenafil

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92
Q

DDx of optic disc edema and RAPD

A

Optic neuritis

AION

CRVO (+/-)

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93
Q

Tx of optic disc atrophy

A

Non

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94
Q

Location of lesion in:

Rt anopsia and left upper quadrantanopsia

A

Rt junctional scotoma

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95
Q

Location of lesion in:

Bilateral hemianopsia

A

Chiasma

Children: craniopharyngioma

Middle ages: pituitary adenoma

Elderly: meningioma

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96
Q

Location of lesion in:

Left homonymous hemianopsia

A

Rt optic tract

More congruent deficit = more posterior lesions

If occipital lesion, macular sparing

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97
Q

Location of lesion in:

Left upper quadrantanopsia

A

Rt temporal lesion

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98
Q

Location of lesion in:

Left lower quadrantanopsia

A

Rt parietal

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99
Q

Location of lesion in:

Homonymous hemianopsia with macular sparing

A

Occipital lesions

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100
Q

If hemiplegia with eyes looking away from hemiplegia, location of lesion?

A

Cerebral hemisphere

Lesion in FEF: can be overcome with doll’s eye maneuver

Seizure involving FEF: eyes deviate away from the focus

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101
Q

Hemiplegia with eyes lookin toward the side of the hemiplagia, location of lesion?

A

Brainstem

Lesion in PPRF

cannot be overcome with doll’s eye maneuver

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102
Q

INO

A

MLF lesion

Gaze away from the side of lesion: ipsilateral adduction defect, contralateral abduction nystagmus

Cannot be overcome by caloric reflect

Accommodation intact

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103
Q

Inv for INO

A

MRI

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104
Q

Inv for diplopia

A

If isolated CN IV or CN VI palsy: observe for a few weeks

If persistent or other symptoms present: W/U

Neuroimaging if:
Bilateral
Multiple nerve involvement
Severe sudden onset headache

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105
Q

Diplopia worstat the end of the day suggests

A

MG

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106
Q

Gaze fixation in peripheral vs central nystagmus

A

Peripheral: relieved with gaze fixation

Central no relief

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107
Q

Direction of nystagmus in peripheral causes

A

Fast phase away from the lesion

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108
Q

If diplopia only on extremes of gase, which eye is pathological?

A

Cover each eye in isolation during extremes of gaze.

The covered eye which makes the lateral image disappear is the pathological one

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109
Q

Clinical manifestations of B12 deficiency

A

The most common initial symptoms:

Paresthesia
Sensory ataxia

Others:

Myelopathy
Weakness with UMN findings
Peripheral neuropathy: distal numbness/paresthesia
Memory impairment
Change in personality
Delirium, confusion
Psychosis
Optic neuropathy

Diarrhea, anorexia

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110
Q

Inv for B12 deficiency

A

Serum cobalamin

Serum methylmalonoc acid

Serum homocysteine

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111
Q

Tx of Vit B12 deficiency

A

Vit B12 IM 1000 microgram/d x 5 d then 1000/mo

Or 1000 oral/d

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112
Q

Folate deficiency symptoms

A

Myelopathy

Peripheral neuropathy

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113
Q

Inv for folate deficiency

A

Serum folate

Serum homocysteine

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114
Q

Copper deficiency symptoms

A

Myelopathy

Pyramidal signs (brisk muscle stretch reflexes)

Severe sensory loss

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115
Q

Copper deficiency inv

A

Serum copper

Ceruloplasmin

Urine copper

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116
Q

Tx of copper deficiency

A

D/C zinc

Oral copper

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117
Q

Vit E deficiency symptoms

A

Ophthalmoplegia

Retinopathy

Spinocerebellar syndrome, cerebellar ataxia

Pripheral neuropathy

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118
Q

Inv for vit E deficiency

A

Serum Vit E

Serum vit E/ Chol+TG

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119
Q

Thiamine deficiency symptoms

A

Beriberi (wet, dry)

Infantile beriberi

Wernicke Korsakoff

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120
Q

Dx of B1 def

A

Clinical

Brain MRI

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121
Q

B6 deficiency symptoms

A

Painful sensoryneural peripheral neuropathy

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122
Q

Dx of B6 deficiency

A

Serum peridoxal phosphate

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123
Q

B3 deficiency

A

Dementia

Encephalopathy

Coma

Peripheral neuropathy

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124
Q

Dx of B3 deficiency

A

Urinary metabolites of niacin

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125
Q

Effect of organic solvents on nervous system

A

Cognitive impairment

Encephalopathy

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126
Q

Effect of pesticides on nervous system

A

Increased risk of Parkinson’s disease

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127
Q

Effect of lead on nervous system

A

Delayed/reversed development

Permanent learning disability

Peripheral neuropathy

Seizures

Coma/death from encephalopathy

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128
Q

Effect of mercury on nervous system

A

Ataxia

Visual loss

Hearing loss

Memory/psychiatric problems

Tiredness

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129
Q

Effect of manganese on nervous system

A

Hallucination

Dystonia

Parkinsonism

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130
Q

Effect of aluminum on nervous system

A

Alzeimer

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131
Q

Effect of arsenic on nervous system

A

Sleeplessness
Sleepiness

irritability

Muscle spasm/fatigue

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132
Q

Neurologic complications of bariatric surgery

A

Deficiencies of fat-soluble and water-soluble vitamins

Should be monitored

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133
Q

The most common cause of late-onset seizures

A

Stroke

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134
Q

Psychiatric symptoms with simple partial vs complex partial seizures

A

Rarely occur with simple partial

More common with complex partial

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135
Q

Awareness in seizure

A

Generalized: loss of awareness

Simple partial: intact

Complex partial: appears awake, but impaired awareness

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136
Q

Petit mal seizure

A

Generalized

Children

Unresponsive 5-10 sec

Arrest of activity, blinking, eye-rolling, staring

3Hz spike and Slow wave activity on EEG

No post-ictal

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137
Q

Grand mal seizure

A

May have prodrome (unease, irritability, hours to days before the episode)

Tonic, clonic, post ictal

Post-ictal: flaccid limbs, extensor plantar reflexes, headache, confusion, aching muscles, sore tongue, amnesia, elevated serum CK, focal paralysis (Todd’s paralysis)

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138
Q

Temporal lobe epilepsy

A

Aura: fear, olfactory/gustatory hallucinations, visceral sensations, déja vu

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139
Q

Frontoparietal cortex seizures

A

Contralateral sensory/motor phenomenon

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140
Q

Alcohol withdrawal seizures

A

Up to 48 h from the last intake

Seizure common

status epilepticus rare

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141
Q

Inv for seizures

A 
CBC
Lytes, Ca, Mg
FBS
ESR
Cr
Liver enzymes
CK
PRL
Toxicology screen
EtOH level
AED level

+/-:
CT/MRI
LP
EEG

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142
Q

Indication for LP in seizure

A

If fever, meningismus

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143
Q

Indication fo imaging in seizure

A

New seizure without identifiable cause

Known seizure history with new neurologic signs/symptoms

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144
Q

Seizures and driving

A

License suspended util 6 mo seizure-free

Longer for commercial drivers

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145
Q

Tx of seizures. Issues to consider

A

Stigma

Educate pt and family

Status of driver’s license

Safety issues

Pregnancy

Avoid precipitating factors

AED

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146
Q

Indications for AED drugs

A

EEG with epileptiform activity

Remote symptomatic cause (organic brain disease, prior head injury, CNS infection)

Abnormal neurologic examination

Abnormal findings on neuroimaging

Nocturnal seizure

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147
Q

Seizure most similar to pseudoseizure

A

Frontal (odd motor activity)

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148
Q

Tongue biting in pseudoseizure

A

At the tip (lateral in seizure)

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149
Q

Motor activity in pseudoseizure

A

Opisthotonos

Rigidity

Eye closure, geotropic eye movement

Irregular extremity movements

Pelvic thrust

Crying

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150
Q

Status epilepticus

A

No return to baseline state for > 5 min

R/O status epilepticus in any pt who is still unconcious > 20 min post-ictal

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151
Q

Complications of status epilepticus

A 
Anoxia
Cerebral ischemia
Cerebral edema
MI
Arrhythmia
Cardiac arrest
Rhabdomyolysis
Renal failure
Aspiration pneumonia/pneumonitis
Death
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152
Q

Initial measures for status epilepticus

A 
ABC
V/S
Monitors
Capillary glucose (STAT)
ECG
nasal O2
IV NS
glucose
IV thiamine
ABG (if respiratory distress/cyanotic)
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153
Q

Blood work for status epilepticus

A 
CBC
Lytes, Ca, PO4, Mg
Glucose
Toxicology 
EtOH
AED levels
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154
Q

Post-treatment stabilization for status epilepticus

A 
CT head
EEG
Foley
Urine toxicology
Monitor for rhabdomyolysis
IV fluid
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155
Q

The most common causes of status epilepticus

A

Failure to take AED

First presentation of epilepsy

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156
Q

Tx fir absence seizures

A

Ethosuximide

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157
Q

Highest risk of teratogenicity with AEDs

A

Valproic acid

Or

2+ concurrent AEDs

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158
Q

Pregnancy with AED

A

Folic acid 5/d preconception

Pre-conception AED levels

Monthly AED levels during pregnancy (maintain preconception levels)

Referal to OB for intrapartum fetal screening

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159
Q

Medication steps in Mx of status epilepticus

A
  1. Lorazepam
  2. Fosphenytoin or phenytoin
  3. Phenobarbital
  4. ICU. Midazolam/propofol/phenobarbital
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160
Q

If suspicious of SAH but normal CT, next step?

A

LP

If normal:
Angiography

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161
Q

Definition of mild NCD

A

Not meeting criteria for major NCD

Measurable deficit in at least one cognitive domain

Reported by pt or others

No impairment of ADLs

non-Amnestic vs Amnestic form, precursor to AD

Pts with mild NCD often troubled by memory symptoms in comparison to pts with dementia

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162
Q

RFs for mild NCD

A

HTN

DM

Obesity

Cardiac disease

Apolipoprotein E epsilon4 genotype

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163
Q

Clinical features of mild NCD

A

Cognitive impairment

Neuropsychiatric symptoms:
Depression, irritability, anxiety, aggression, apathy

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164
Q

Investigations for mild NCD

A

Establish a baseline for F/U

Clinical interview with pt and caregiver (cornerstone)

Neuropsychological testing: MMSE, MoCA (should not be used in isolation)

neuroimaging: non-contrast brain CT

Exclude treatable conditions

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165
Q

If abnormal neuropsychiatric testing, next step?

A

F/U in 1 y

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166
Q

Tx of mild NCD

A

Watch and wait

No evidence for anything!!

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167
Q

Cognitive domains

A

Complex attention

Language

Memory and learning

Executive function

Perceptual-motor

Social cognition

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168
Q

Head turning sign

A

Pt looks at caregiver for answers after being asked a question in clinical interview

Seen in cognitive impairmant

169
Q

Inv fir NCD

A 
CBC
Glucose
TSH
B12
RBC folate
Lytes
LFT
Renal function
Lipid
Ca
CT head
MRI
SPECT
\+/- 
VRRL
HIV
ANA
Anti-dsDNA
ANCA
Ceruloplasmin
Copper
Cirtisol
Tixicology
Heavy metals
170
Q

Alzheimer disease sumptoms

A

Memory impairment

Aphasia

Apraxia

Agnosia

171
Q

Symptoms of dementia with lewy bidy

A

Visual hallucination

Parkinsonism

Fluctuating cognition

172
Q

Frontotemporal dementia (pick)

A

Behavioral: disinhibition, perseveration,
Decreased social awareness, mental rigidity

Memory relatively spared

Language: progressive non-fluent aphasia, santic dementia

173
Q

Vascular dementia features

A

Bradyphrenia ( without parkinsonism): slow thinking, slow learning, slow gait

dysexecutive syndrome

Abrupt onset

Stepwise deterioration

Progressive deterioration more common

174
Q

Clinical features of syphilis dementia

A

Ataxia

Tabes dorsalis

Myoclonus

175
Q

Dementia with myoclonus

A

CFJ

Syphilus

176
Q

Ab positive in neoplastic dementia

177
Q

Typical presentation if AD

A

Mild phase:
Impaired memory and learning
+/- deficit in executive function

Mod-sev phase:
Visuoconstructional
Peceptual-motor
Language

Anterograde amnesia, Aphasia, Apraxia, Agnosia, Disturbance in executive function

178
Q

RFs for AD

A

Age (the largest RF)

Down syndrome

E4 polymorphism for APOE

FHx

Traumatc brain injury

Low education

Vascular RFs

179
Q

AD pathology

A

Senile plaques (extracellular, grey matter)

Loss of synapses

Neurofibrillary tangles

Loss of cholinergic neurons in Meynert

180
Q

AD clinical features

A 
Cognitive impairment:
Memory for newly acquired information
Language
Abstract reasoning
Executive function

Behavior and psychiatric manifestations:
MDD/Apathy
Psychosis, irritability, agitation, combativeness, wandering

Motor manifestations:
Gait, dysphagia, incontinence, myoclonus, seizures

182
Q

Inv for AD

A

EEG: may show generalized slowing

MRI: preferential atrophy of hippocampi and precuneus of parietal lobe, dilation of lateral ventricles, widening of cortical sulci

SPECT: hypoperfusion in temporal and parietal lobes

PET: using PIB as a tracer to image beta-amyloid plaque

183
Q

Tx of AD

A

Acetylcholinesterase inhibitors:
Donepezil
Rivastigmine
Galantamine

NMDA-receptor antagonist:
Memantine (for later stages)

Neuroleptics (agitation)

Trazodone (sleep disturbance)

SSRI

Redirection, behavior modification, family support, day car facilities

184
Q

Effect of Acetylcholinesterase inhibitors in AD

A

Slow cognitive decline

Improve morbidity

Do not prolong life expectancy

185
Q

Acetylcholinesterase inhibitors contraindications

A 
Relative:
Bradycardia
Heart block
Arrhythmia
CHF
CAD
Asthma
COPD
Ulcers
RFs for ulcers/ GIB
186
Q

Cognitive effect of atypical antipsychotic meds

A

Long-term use for behavioural symptoms, associated with greater rate of cognitive decline

187
Q

NCD with Lewy body features

A

Early:
Impaired complex attention,
Impaired executive function

Complex visual hallucinations

Fluctuating cognition

Parkinsonism (resting tremor may be absent)

REM sleep behavior disorder

Severe sensitivity to neuroleptic meds (NMS, rigidity, extrapyramidal symptoms)

Repeated fall/syncope/loss of consciousness

Hallucination (auditory)/ delusion/ depression

188
Q

Lewy body dementia pathology

A

Eosinophilic intracytoplasmic inclusions

Both cortical and subcortical structures

189
Q

Inv in Lewy body dementia

A

CT/MRI:
Relative preservation of medial temporal structures

SPECT/PET: low striatal dopamine transporter uptake

190
Q

Tx of Lewy body dementia

A

Acetylcholinesterase inhibitors

191
Q

frontotemporal dementia movement disorder

A

Corticobasal degeneration

Progressive supranuclear palsy

192
Q

Pathology of FTD

A

Severe atrophy

Gliosis, swollen neurons, microvacuolation , Specific neuronal inclusion bodies

Atrophy in frontal and anterior temporal lobes

193
Q

Vascular NCD clinical features

A

Onset of cognitive disease temporally related to one or more cerebrovascular events.

Decline in complex attention

Decline in frontal executive function

Personality and mood changes

Abulia (absence of will power)

Depression

Emotional lability

Psychomotor slowing

194
Q

RFs for vascular NCD

A 
HTN
DM
Smoking
Obesity
High cholesterol
High homocysteine 
RFs for AF
195
Q

Second most common cause of NCD

A

Vascular

Higher prevalence in African-Americans

M>F

196
Q

CJD

A

Prion

Spongiform changes, astrocytosis, neuronal loss

Sporadic > hereditary

197
Q

Inv for CJD

A

CSF analysis

MRI brain : cortical/ subcortical FLAIR

EEG: periodic complexes

Brain Bx: definitive Dx

198
Q

Tx of CJD

199
Q

Broca’s area

A

Posterior inferior frontal lobe

Language production

200
Q

Wernicke’s area

A

Posterior superior temporal lobe

Language comprehention

201
Q

Angular gyrus

A

Relays written visual stimuli to Wernicke’s area

Reading comprehension

202
Q

Arcuate fasciculus assiciation bundle

A

Connects Wernicke and Broca

203
Q

Aphasia localizes the lesion to which hemisphere?

A

Dominant hemisphere

204
Q

Broca’s aphasia:

A

Non-fluent

Good comprehension

Poor repetition

Poor naming

205
Q

Wernicke’s aphasia

A

Fluent

Poor comprehension

Poor repetition

Relatively spared naming

206
Q

Apperceptive visual agnosia

A

Distorted visual perception.

Bilateral temporo-occipital cortex

207
Q

Impaired streognosis

A

Inability to identify by touch

Anterior parietal lobe (in the hemisphere opposite the affected hand)

208
Q

Prosopagnosia

A

Inability to recognize familiar faces

Bilateral temporo-occipital

209
Q

Hallmarks of brain concussion

A

Confusion and amnesia

210
Q

Loss of consciousness in concussion

A

Must be less than 30 min

Initial GCS must be 13-15

Post-traumatic amnesia must be <24h

211
Q

Does extent of retrograde amnesia correlate with severity of concussion?

212
Q

Dominant parietal lobe lesion symptoms

A

Acalculia

Agraphia

Finger agnosia

Left-right disorientation

213
Q

Non-dominant parietal lobe lesion

A

Neglect

Anosognosia (loss of self-awareness)

Asomatognosia (loss of recognition or awareness of part of the body)

214
Q

Indications for hospitalization of concussion

A

GCS < 15

Seizures

Bleeding diathesis

Abnormal CT

215
Q

Inv for concussion

A

Neurological exam

Neurocognitive assessment

+/-
Skull Xray
CT
MRI

216
Q

Tx of concussion

A

Observe for 24 h in all pts

If any loss of consciousness/oersistent symptoms, -> ED

Early rehabilitation (PT, OT, SLP, vestibular therapy, driving, therapeutic recreation)

Meds for headache, pain, depression

CBT

Relaxation therapy

217
Q

Post-concussion syndrome

A

Dizziness
Headache
Neuropsychiatric symptoms
Cognitive impairment

Resolves within weeks to months

218
Q

Post-traumatic headache starts within

219
Q

Post-traumatic epilepsy

A

2% prevalence

Not prevented by prophylactic anticonvulsants

220
Q

Frontotemporal NCD features

A

Behavioral variant(more common):

Behavioral disinhibition

Apathy or inertia

Loss of sympathy/empathy

Preservative, stereotyped or compulsive/ritualistic behavior

Hyperorality and dietary changes (binge eating, increased consumption of alcohol/cigarette, inedible objects)

Language variant:
Decline in language ability (speech production, word finding, object naming, grammar, word comprehension)

221
Q

Location of lesion in hemiballismus

A

Vascular lesion of the contralateral subthalamic nucleus

222
Q

DDx of resting tremor

A

PD
parkinsonism
Wilson
Mercury poisoning

223
Q

DDx of Action-postural tremor

A 
Physiologic
Essential
Hyperthyroidism
Hypoglycemia
Heavy metal poisoning
CO poisoning
Drug toxicity
Sedative/alcohol withdrawal
224
Q

DDx for Action-Intention tremor

A 
Cerebellar disorders
Wilson
MS
AED
Alcohol
Sedatives
225
Q

Tx of resting tremor

A

Carbidopa-levodopa

Surgery

DBS

226
Q

Tx of postural tremor

A

Propranolol

Primidone

Topiramate

AED

227
Q

Tx of intention tremor

A

Treat underlying cause

228
Q

Hiccup movement disorder

A

Physiologic myoclonus

229
Q

Infectious disease with myoclonus

A

CJD

AIDS-Dementia

230
Q

Inv in young pt with tremor

A

TSH
Ceruloplasmin
CT/MRI
…

231
Q

Most common cause of chorea

A

Drug therapy for PD (L-dopa)

232
Q

RFs for PD

A

FHx

Male

Head injury

Rural living

Exposure to certain neurotoxins

233
Q

Protective factors against PD

A

Coffee

Smoking

NSAIDs

Estrogen replacement in post-menopausal women

234
Q

Location of pathology in PD

A

Decreased dopaminergic neurons in pars compacta of substantia nigra

235
Q

Speech in PD

A

Aprosody (monotonus)

Hypophonia

Dysarthria

236
Q

Writing in PD

A

Micrographia

237
Q

Gait in PD

A

Shuffling

Decreased arm swing

Freezing of gait

Postural instability (late)

238
Q

Bradyphrenia

A

Slow to think or respond

Seen in PD

239
Q

Tx of Parkinson’s disease

A

Mainstay:
levodopa/carbidooa
Or
Levodopa/benserazide

Early:
dopamine agonist
Amantadine
MAOI

Adjunct: 
Dopamine agonists
MAOI
Anticholinergics (esp if tremor)
COMT inhibitors
240
Q

Surgical Tx for PD

A

Thalamotomy
Pallidotomy
DBS

241
Q

Psychiatric treatment for PD

A

SSRIs
(First line)

TCA (fall risk, cognitive impairment, worsening symptoms of PD)

242
Q

Progressive supranuclear palsy

A

Parkinsonian disorder with limited vertical gaze (downgaze more specific)

Early falls

243
Q

Corticobasal syndrome

A

Unilateral parkinsonism

Alien limb

244
Q

Multiple system atrophy (Shy-Drager)

A

Cerebellar or parkinsonian symptoms

+ early autonomic dysfunction

245
Q

Vascular parkinsonism

A

Multi-infarct presentation

Gait instability

Lower body Parkinsonism

Tremor less likely

246
Q

Dopamine agonist vs Levodopa for PD

A

Dopamine agonists have:

Fewer motor side effects
Worse symptom control
Increased other side effects

247
Q

Atypical parkinsonism features (consider other diagnoses)

A

Poor response to levodopa

Abrupt onset of symptoms

Rapid progression

Early falls

Early autonomic dysfunction

Symmetric symptoms at onset

Early age of onset (<50y)

Early cognitive impairment

FHx of psychiatric/dementing disorders

Recent diagnosis of psychiatric disease

Hx of encephalitis

Unusual toxin exposure

Extensive travel Hx

248
Q

Huntington disease

A

Heredity: AD

Pathology: accumulation of abnormal protein in neurons. Global cerebral atrophy

Onset: 35-44 yr

249
Q

Symptoms of huntington

A 
Insidious
Clumsiness
Fidgetiness
Irritability
Progression
Psychosis, NCD, chorea
Depression, impulsivity, bouts of violence
250
Q

Chorea in huntington disease

A

Movement of eyebrows and shoulders

Progression to dance-like ballism

Dystonia, rigidity in late stages

251
Q

Inv for Huntington

A

MRI:
Atrophy of cerebral cortex and caudate nucleus.
Enlarged ventricles

Genetic testing (CAG repeat in HTT gene on chromosome 4)

252
Q

Tx of Huntington

A

No disease altering Tx

Psychiatric Sx: anti drpressant, anti paychotic

Chorea: neuroleptic, BDZ

Dystonia: botulinum toxin

253
Q

Most common movement disorders

A

PD > essential tremor > dystonia

254
Q

Dystonia

A

Co-contraction of agonist-antagonist muscles

255
Q

Factors exacerbating/ relieving dystonia

A

Exacerbation:
Fatigue

Stress

Emotion

Relief:
Sleep

Specific tactile/proprioceptive stimuli

256
Q

Poor prognostic factors for dystonia

A

Young age

Leg dystonia

257
Q

Tx of dystonia

A

Local meds: botulinum toxins

Systemic meds: 
Benztropine (anticholi)
Baclofen ( muscle relaxant)
BDZ
Dopamine depletors (tetrabenazine)
Dopamine (for dopa-responsive dystonia)
Surgical:
Denervation of affected muscle
Stereotactic thalatomy
Posteroventrsl pallidotomy
DBS
258
Q

Criteria for tic

A

Present for an extended period of time

Onset before 18

Not attributable to substance effect/ medical condition

259
Q

Tic types

A

Tourette syndrome:
Both motor and vocal tics for more than 1 yr

Persistent motor/vocal tic disorder (not both) more than 1 yr

Provisional tic disorder: less than 1 yr

Secondary tic disorder: trauma, CJD, encephalitis, drugs, Sydenham, mental retardation syndromes.

260
Q

Tic Tx

A

Dopamine blocker

Dopamine depletor

Clonidine

Clonazepam

DBS

261
Q

Tourette Syndrome

A

Both multiple motor and one or more vocal tics (not necessarily concurrently)

May wax and wane

Can be suppressed voluntarily.

Preceded by unpleasant sensation

> 1yr

No tic-free period for more than 3 mo

Onset before 18 (4-6 yr)

Not due to substance/ medical condition

M>F

Associated with: OCD, ADHD, rages, sleep-wake disturbances, learning disabilities

50% tic-free by 18

262
Q

Cerebellar dysfunction symptoms

A

Nystagmus (gaze evoked)

Dysarthria (scanning/slurred speech)

Ataxia: broad based, uncoordinated, lurching

Dysmetria

Dysdiachokinesia

Postural instability: truncal ataxia, titubation, difficulty with tandem

Intention tremor

Hypotonia

Pendular patellar/triceps reflex

Rebound phenomenon (overcorrection of displaced limb)

Hypometric/hypermetric saccades

263
Q

Which part of brain is affected in Wernicke-Korsakof?

A

Cerebellum

264
Q

Friedrich ataxia

A

Gait ataxia

Limb ataxia

Weakness

Areflexia

Extensor plantar reflex

Impaired proprioception and vibration

Dysarthria

Cardiomyopathy

Kyphoscoliosis

265
Q

Spinocerebellar ataxia

A

AD

Ataxia

Dysarthria

Chorea

Polyneuropathy

Pyramidal Sx

Extrapyramidal Sx

Dementia

CAG repeats (most common type)

266
Q

ALS pathology site

A

Anterior horn cells of spinal cord

Cranial nerve nuclei

Corticospinal tract

267
Q

ALS Sx

A

UMN and LMN

Dysarthria

Dysphagia

Tongue atrophy and fasciculation

Facial weakness and atrophy

Pseudobulbar affect

Frontotemporal dementia

Sparing of: sensation, ocular muscles, bowel, bladder, fasciculation

268
Q

Inv for ALS

A

EMG:
Chronic denervation and re-innervation
Fasciculation

NCS:
R/O peripheral neuropathy

CT/MRI:
R/O cord disease/compression

269
Q

Interventions in ALS which can extend survival

A

Riluzole

BiPAP

270
Q

Tx of ALS

A

Riluzole (slows disease progression)

For spasticity/cramping:
Baclofen, tizanidine, regular exercise, PT

Sialorrhea:
TCA, sublingual atropine, parotid/submandibular botox

Pseudobulbar affect:
Dextrometorphan/quinidine, TCA, SSRI

Non-pharmacologic:
High caloric diet, 
ventilatory support (BiPAP)
Early nutritional support
Rehabilitation
Psychosocial support
271
Q

Red flags inconsistent with ALS

A

Sensory Sx

Predominant pain

Bowel/bladder incontinence

Cognitive impairment

Ocular muscle weakness

272
Q

Progressive muscular atrophy

A

Only LMN Sx

Later onset than ALS

273
Q

Primary muscular atrophy

A

UMN

later onset than ALS

Not fatal

274
Q

Spinal muscular atrophy

A

Pediatric

Symmetric LMN

275
Q

Infection DDx of ALS

A

Post-Polio syndrome

West Nile

276
Q

Diabetic neuropathies

A

Peripheral neuropathy:
Glove and stocking pattern (pain, numbness)

Autonomic:
Anhidrosis, 
Orthostatic hypotension
Impotence,
Gastroparesis,
Bowel/bladder dysfunction

Mononeuropathy multiplex:
Infarct, compression

Cranial neuropathy:
CN III (pupil sparing) > IV > VI

Lumbosacral plexopathy

277
Q

Pattern of poly neuropathy

A

Stocking-glove sensorymotor deficit

Symmetrical

Diseases affecting longer fibers first

DDx:
DM, Renal disease, substances, toxins, genetics, SLE, HIV, leprosy, alcohol, B12 deficiency, uremia

278
Q

Chronic inflammatory demyelinating polyneuropathy

A

Chronic

Relapsing

Sensory motor

Increased CSF protein

Demyelination

Fluctuating course

Tx:
1st line: prednisone
Others: plasmaphresis, IVIG, azathioprine

279
Q

Inv for polyneuropathy

A

Glucose
B12 level with metabolites
SPEP
Serum protein immunofixation

280
Q

The most common antecedent infection in GBS

A

Campylobacter jejuni

281
Q

GBS

A

Acute

Rapidly evolving

Demyelinating

Inflammatory. (AI attack to myeline)

Polyradiculoneuropathy

Starts in the distal lower limbs and ascends

282
Q

GBS Sx

A

Sensory:
Distal symmetric paresthesias
Loss of proprioception and vibration sense
Neuropathic pain

Motor:
Weakness. Starting distally in legs. Areflexia.

Autonomic:
Blood pressure dysregulation
Arrhythmias
Bladder dysfunction

283
Q

Inv for GBS

A

EMG/NCV:
Conduction block
Slowing (motor > sensory)
Sural sparing

284
Q

Tx of GBS

A

IVIG

Plasmaphresis

Pain management

Monitor vital signs and vital capacity

285
Q

Course of GBS

A

Peak: in 2-3 weeks

Resolution: 4-6 weeks

286
Q

Miller-Fischer

A

Variant of GBS

Ophthalmoplegia
Ataxia
Areflexia

287
Q

Fatigability test

A

Holding the arms out

Holding the gaze in the upward position

Improves with: rest, ice

288
Q

Myasthenia gravis pathogenesis

A

AI against AChR or Musk (anti-AChR or anti-Musk Ab)

15% thymic neoplasm

85% thymus hyperplasia

289
Q

MG age of onset

A

F: 20s

M: 60s

290
Q

MG Sx

A

Symmetric/Asymmetric proximal weakness

Fatigable

No reflex changes

No sensory changes

No anticholinergic Sx

No coordination abnormality

Diplopia/prosis (ocular)

Dysarthria/dysphagia (bulbar)

Respiratory muscle weakness

291
Q

Factors exacerbating MG

A

Infection

Pregnancy

Menses

Various drugs

292
Q

Inv for MG

A

Edrophonium (Tensilon) test

EMG (decremental response on repeating)

Spirometry (use forced vital capacity to follow adequacy of respiratory efforts)

Anti-AChR (70-80 % sensitivity). If negative, Anti-MuSK

CT/MRI for thymoma/thymic hyperplasia

293
Q

Tx of MG

A

Thymectomy

Acetylcholine esterase inhibitor: pyridostigmine. (Symptomatic relief)

Mainstay: steroids.

Others: AZA, CyP, MMF (adjunct. Steroid sparing)

For crisis:
IVIG, plasmaphresis

294
Q

Lambert-Eaton Myasthenic Syndrome pathogenesis

A

AI

Ab against presynaptic voltage-gated Ca channels

Decreased ACh release at the NMJ

50-66% associated with SCC of the lung

295
Q

Lambert-Eaton Myasthenic Syndrome Sx

A

Weakness, esp proximal lower

No sensory Sx

No coordination Sx

Reflexes: diminished or absent

Reflexes increase after active muscle contraction

Bulbar Sx, Ocular Sx (less often than MG)

Autonomic symptoms (anti-cholinergic), esp dry mouth

Fatigability

296
Q

Inv for Lambert-Eaton Myasthenic Syndrome

A

Edrophonium test: no response

EMG: incremental response to repetitive stimulation

Screen for malignancy

297
Q

Tx of Lambert-Eaton Myasthenic Syndrome

A

Tumor removal

3,4-diaminopyridine
Pyridostigmine

Steroids
Plasmaphresis
IVIG

298
Q

Most common form of botulism

A

Infantile

Honey or corn syrup ingestion

299
Q

Botulism Sx

A

Onset: 6-48 h after ingestion

CN paralysis:
Ptosis
Extraocular muscle weakness
Dilated, poorly reactive pupils
Dysarthria
Ja weakness
Dysphagia
Autonomic dysfunction:
Nausea
Orthostatic hypotension
Constipation
Bladder distention

Anticholinergic:
Dry mouth…

Symmetric weakness, paralysis

DTR: absent/decreased

300
Q

Pattern of paresis in botulism

A

Starts with GI symptoms

Then extraocular muscles

Then dysphagia

Then limbs and resporatory

All associated with dry mouth

301
Q

Inv for botulism

A

Blood test for toxin

Stool culture

CT/MRI to R/O stroke, lesion

302
Q

Tx of botulism

A

Anti-toxin

Supportive

303
Q

Bx of different myositis

A

Polymyositis: endomysial infiltrate

Dermatomyositis: perifascicular atrophy

Inclusion body myositis: inclusion body

304
Q

Endocrinopathies causing myopathy

A

Hypo/hyperthyroidism

Hypo/hyperparathyroidism

Cushing

305
Q

Key feature of inclusion body myositis

A

Weakness of quadriceps and deep finger flexors

306
Q

Critical pt myopathy

A

ICU

Hx of steroids/nom-depolarizing paralyzing agent

Bx: selective loss of myosin

307
Q

Meds causingmyopathy

A 
Steroids
Statins
Anti-retrovirals
Thyroxine
Fibrates
Cyclosporine
Ipecac

Ethanol
Cocaine
Heroin

308
Q

McArdle myopathy

A

Herditary metabolic

Exercise-related myalgia, cramping, myoglobinuria

Increase lactate

Increased serum/urine myoglobin

(Post-exercise)

309
Q

Most common adult muscular dystrophy

A

Myotonic dystrophy

310
Q

Myotonic dystrophy

A

AD

unstable CTG repeats (number correlates with severity)

311
Q

Myotonic dysthrophy Sx

A

Ptosis

Bifacial weakness

Frontal baldness

Triangular face (drooping/dull appearance)

312
Q

Pattern if weakness in myotonic dystrophy

A

Distal weaker than proximal

Steppage gait

Delayed relaxation of muscle after exertion

Myotonia test: tapping on tenar muscles with hammer

Cardiac conduction defect in 90%

Hypoventilation 2° to muscle weakness

Subcapsular cataract

Retinal degeneration

Decreased intraocular pressure

DM, infertility, testicular atrophy

313
Q

Inv for myotonic dystrophy

314
Q

Myotonic dystrophy Tx

A

No cure

Progressive

Death around 50

Phenytoin for myotonia

315
Q

Adjuvant treatments for pain

A 
TCA
SSRI
AED: gabapentin, pregabalin, carbamazepine
Baclophen
Phenoxybenzamine
Clonidine
316
Q

Mx of neuropathic pains

A

Treat underlying

1st line:
Gabapentinoids, TCA, SNRI

2nd line:
Tramadol, opioid analgesics

3rd line:
Cannabinoids

4th line:
Topical lidocaine (2nd line for PHN)
Methadone
Lamotrigine
Locasamide
Tapentadol
Botulinum toxin

Non-pharma:
CBT, psychotherapy, PT

317
Q

Trigeminal neuralgia territory

A

V3 > V2&raquo_space; V1

F> M

Middle aged, elderly

318
Q

Etiology of Trigeminal neuralgia

A

Idiopathic

Compression by tortuous blood vessels (SCA)

CPA tumor

MS

Secondary causes more likely if: bilateral or sensory loo

319
Q

Inv for Trigeminal neuralgia

A

1st line:
Carbamazepine
Oxcarbazepine

2nd line:
Baclofen
Lamotrigine

Surgery if resistant

320
Q

Distribution of PNH

A

Thoracic, trigeminal, cervical > lumbar > sacral

321
Q

Pathogenesis of PHN

A

Destruction of sensory ganglion neurons (dorsal root, trigeminal, geniculate)

322
Q

RFs for developing PHN

A

Older age

Greater acute pain

Greater rash severity

323
Q

Prevention of PHN

A

Varicella vaccine in childhood

Herpes zoster vaccine after 60

324
Q

Tx of PHN

A 
TCA
Pregabalin
Gabapentin
Opiates
Lidocaine patch
Intrathecal methylprednisolone
Topical capsaicin

Surgical

Early treatment of zoster with antivirals

CS does not decrease PHN

325
Q

Pain in DM. First thing toconsider?

A

Is pain neuropathic or vascular)

Neuropathic: present at rest, improved with walking, sharp/tingling, more in feet than calves

326
Q

Tx of diabetic neuropathic pain

A

Level A: pregabalin

Level B: venlafaxine, duloxetine, amitriptyline, gabapentin, valproate, opioids, capsaicin

327
Q

Complex regional pain syndrome Sx

A

An initiating noxious event (MI, stroke)

Disproportionate pain, allodynia, hyperalgesia

Edema, changes in skin blood flow, abnormal vasomotor activity, osteoporosis, hyperhidrosis, hair loss, fascial thickening

328
Q

Types of CRPS

A

Type I: minor injuries of limb or lesions in remote body areas precede onset of pain (reflex sympathetic dystrophy)

Type II: injury of peripheral nerves precedes the onset of syndrome

329
Q

Inv for CRPS

A

Trial of differential neuronal blockade

Autonomic testing (sympathetic dysfunction)

Bone scan

Plain Xray

MRI

330
Q

Tx of CRPS

A

Goal: to facilitate function

Education

Support groups

PT/OT

Smoking cessation

Topical capsaicin
TCA
NSAIDs
CS/lidocain injection in tender points
Gabapentin/ pregabalin/lamotrigine
Calcitonin
Bisphosphonates
Oral CS

Surgery

Pain management clinic

331
Q

Headache red flags

A

New-onset headache

Quality worse/different than previous headaches

Sudden and severe (thunderclap)

Immunocompromised

Fever

Focal neurological deficits

Trauma

Papilledema

Altered LOC

meningismus

332
Q

Tension headache Sx

A

F>M

Worse in PM

Bilateral frontal/ Nuchal-occipital

Band-like, constant

Triggers: depression, anxiety, noise, hunger, sleep deprivation

Relieved with rest

333
Q

Tx of tension headache

A

Psychological counseling

Physical modalities (heat, massage)

Simple analgesics
TCA

334
Q

Migraine Sx

A

F>M

FHx +++

Unilateral > bilateral
Fronto-temporal

N/V, photo/phonophobia, aura

Worse in PM

Throbbing

Triggers: noise/light, caffeine/alcohol, hunger, stress, sleep deprivation/excess, chocolate, tyramine, nitrite, hormonal changes

Relief with: rest

335
Q

Acute Tx of migraine

A

ASA
NSAIDs
Triptans
Ergotamine

336
Q

Prophylaxis for migraine

A

TCA
AED (valproate, topiramate)
Propranolol

337
Q

Cluster headache Sx

A

M>F

FHx +

Retro-orbital

Early AM or late PM

Wakes from sleep

Worse with light, EtOH

Palliation with: walking around

Red watery eye, nasal congestion, rhinorrhea, unilateral horner

338
Q

Tx of acute cluster headache

A

O2

Sumatriptan (nasal, injection)

339
Q

Prophylaxis for cluster headache

A

Verapamil

Lithium

Methylsergide

Prednisolone

340
Q

Headache with Horner

341
Q

Headache worse by caffeine

342
Q

Headache worse By EtOH

343
Q

Headache worse by hunger

A

Migraine

Tension

344
Q

Headache prevented by prednisolone

345
Q

Headache prevented by lithium

346
Q

Headache prevented by TCA

A

Migraine

Tension

347
Q

Headache due to meningeal irritation is worse in which time of the day?

A

AM

Provoked by: head movement

348
Q

Drugs triggering migraine

A

Estrogen

Nitroglycerin

349
Q

Migraine aura

A

Fully reversible

Focal cerebral dysfunction

Lasts < 60 min

350
Q

Waking state characteristics

A

EEG: Alpha wave (high frequency, low voltage)

EOG:rapid, blinking

Muscle tone: high

351
Q

Stage N1 sleep characteristics

A

EEG: alpha < 50% + slow wave

EOG: slow, roving

Muscle tone: High, gradually droping

352
Q

Stage N2 sleep characreristic

A

EEG: K complex. Sleep spindles

EOG: still

Muscle tone: high

353
Q

Stage N3 sleep characteristics

A

EEG: Delta waves (low frequency, high voltage)

EOG: still

Homeostatic sleep.
Reduced BP, HR, CO, RR.
Growth hormone release.

354
Q

REM characteristics

A

EEG: sawtooth, mixed frequencies, low voltage

EOG: rapid eye movement

Muscle tone: very low

Irregular respiration
Arrhythmias
Heart rate variation
Classical dreaming state

355
Q

Dreaming happens in which state of sleep?

356
Q

Effect of BDZ in sleep

A

Reduce slow wave sleep

357
Q

Effect of antidepressants (TCA, SSRI, MAOI) on sleep

A

Prolong REM latency

Reduce REM

358
Q

Effect of alcohol on sleep

A

Hastens sleep onset

Associated with increased arousals

359
Q

Etiology of RLS/PLMS

A

Central (spasticity)

Peripheral (radiculopathy, plexopathy)

Pregnancy

Iron deficiency

Alcohol use

B12 deficiency?

360
Q

Tx of RLS/PLMS

A

Remove underlying (iron, B12)

1st line: dopaminergic agonists

Clonazepam (causes tachyphylaxis)

Opioids (exceptional curcumstances)

DO NOT USE: levodopa/carbidopa (worsens)

361
Q

Narcolepsy Sx

A

Narcolepsy

Cataplexy

Sleep paralysis

Hypnogogic hallucination

362
Q

Onset of narcolepsy

A

Adolescence/early adulthood

Lifelong

363
Q

Etiology of narcolepsy

A

AI attack on orexin/hypocretin system

MS

Head trauma

Hypothalamic tumors

Familial

364
Q

Dx of narcolepsy

A

Hx

Sleep latency test: short sleep latency < 8 min

REM within 15 min of sleep onset

365
Q

Tx of narcolepsy

A

Sleep hygiene

Scheduled brief naps

Restricted driving

Alerting agents: modafinil

Stimulants: methylphenidate

Anticataplectic:
TCA, SSRI, sodium oxybate

366
Q

In elderly REM sleep behavior disorder may be associated with

367
Q

In children, slow wave sleep arousal may be associated with

A

Sleep disordered breathing

368
Q

Amaurosus fugax

A

Transients monocular painless vision loss (TIA)

369
Q

Hypertensive encephalopathy Sx

A

BP > 200/130

Abnormal fundoscopic exam:
Papilledema
Exudate
Cotton wool
Hemorrhage

Focal neurological symptoms

N/V

Visual disturbances

Change in LOC

370
Q

Stroke mechanism in pts with chronic DM or HTN

A

Small vessel/lacunar

Due to vessel wall thickening

Mainly small penetrating arteries

Basal ganglia, internal capsule, thalamus

371
Q

Most common cause of ICH

A

HTN

Esp in: putamen, thalamus, pons, cerebellum

372
Q

Cerebral venous thrombosis Sx

A

Headache

Focal neurological deficit

CN palsies

Seizures

Dx: MRV, CTV

Tx: heparin then warfarin

373
Q

ACA Stroke symptoms

A

Contralateral leg paresis/sensory loss

Cognitive deficit: apathy, confusion, poor judgment

374
Q

MCA stroke Sx

A

If proximal:

Contralateral weakness/sensory loss of face and arm

Cortical sensory loss

Contralateral homonymous hemi/quadrantanopia

Aphasia (if dominant hemisphere)

Neglect (if non-dominant hemisphere)

Eye deviation towards the side of lesion

375
Q

PCA stroke

A

Contralateral hemi/quadrantanopsia

Midbrain findings:
CN III, CN IV palsy
Pupillary changes
Hemiparesis

Thalamic findings:
Sensory loss
Amnesia
Decreased level of consciousness

If bilateral:
Cortical blindness
Prosopagnosia

Hemibalismus

376
Q

PICA stroke Sx

A

Lateral medullary or Wallenberg syndrome

Ipsilateral ataxia
Ipsilateral Horner
Ipsilateral facial sensory loss
Contralateral limb pain and temperature impairment
Nystagmus
Vertigo
N/V
Dysphagia
Dysarthria
Hiccup
377
Q

Basilar artery stroke Sx

A 
Proximal:
Impaired EOM
Vertical nystagmus
Reactive myosis
Hemi/quadriplegia
Dysarthria
Locked-In syndrome
Coma

Distal:
Somnolence
Memory/behavior abnormalities
Oculomotor defect

378
Q

Medial medullary infarct Sx

A

Anterior spinal artery

Contralateral hemiparesis (facial sparing)

Contralateral impaired proprioception/vibration

Ipsilateral tongue weakness

379
Q

Lacunal infarcts

A

Posterior limb of internal capsule:
Pure motor hemiparesis: contralateral arm, leg, face

Ventral thalamic:
Pure sensory loss: hemisensory loss

Ventral pons or internal capsule:
Ataxic hemiparesis: Ipsilateral ataxia and leg paresis

Ventral pons or genu of internal capsule:
Dysarthria, facial weakness, dysphagia, mild hand weakness/clumsiness

380
Q

Inv for stroke

A

Capillary glucose

Non contrast CT

ECG

Carotid doppler, echocardiogram

CBC, lytes, Cr, blood glucose, lipid profile, PTT/INR

+/- MR/CT angio

381
Q

CT Findings in stroke

A

Loss of white-gray differentiation

Sulcal effacement

Hypodensity of paranchyma

Insular ribbon sign

Hyperdense MCA sign

382
Q

Acute stroke management

A

ABC

V/S monitoring

Capillary glucose

rtPA within 4.5 h of ischemic stroke

Anti-platelet:
At presentation, if rtPA not given
After 24 h, if rtPA given

Anti-coagulant:
If AF and rtPA not received. IV heparin. Then warfarin.

Early thrombectomy if large artery occlusion of the proximal anterior occlusion

383
Q

Hyperglycemia in stroke

A

Can increase infarct size.

Avoid hyperglycemia

384
Q

Stroke and fever

A

Think septic amboli

Lower temperature

385
Q

Stroke and dysphagia

386
Q

Bed bound stroke pt

387
Q

Stroke and HTN

A

DO NOT LOWER BP

D/C anti-hypertensives for 48-72 h

Tx if:
BP > 220/120
Acute MI
Renal failure
Aortic dissection

1st line: IV labetalol

388
Q

Contraindications to rtPA

A 
Improving Sx
Minor Sx
Seizure at stroke onset
Recent major surgery or trauma (within 14 d)
Recent GI/urinary hemorrhage (within 21 d)
Recent LP
Recent arterial puncture at non-compressible site
PMHx of ICH
Sx of SAH/MI/pericarditis
Pregnancy
sBP > 185
dBP > 110
Aggressive Tx to decrease BP
Uncontrolled serum glucose
Thrombocytopenia
Hemorrhage or mass on CT
High INR or aPTT
389
Q

Etiological Dx

A

Critical for secondary prevention

MRI

CTA/MRA

Echo

Holter

390
Q

Prevention of ischemic stroke with anti-platelet therapy

A

Primary prevention:
No firm evidence in low-risk pt without prior history

Secondary prevention:
Initial choice: ASA
if ineffective or contra: aggrenox, clopidogrel

391
Q

Prevention of ischemic stroke in pt with carotid stenosis

A 
Primary prevention (asymptomatic pt):
Carotid endarterectomy controversial

Secondary prevention:
Clearly beneficial in symptomatic pts with severe stenosis 70-90%
Less beneficial for moderate stenosis (50-69%)

392
Q

Prevention of ischemic stroke in pt with AFib

A

CHADS2

0: antiplatelet
1: antiplatelet or anticoagulation

2 and higher: anticoagulation

Warfarin (INR 2-3), Factor X inhibitor, dabigatran

393
Q

Prevention of ischemic stroke in pt with HTN

A

Primary prevention:
Target: < 140/90. If DM or renal disease, < 130/80. If high risk pt, < 120.

ACEI

Secondary prevention:
ACEI and thiazide

394
Q

Prevention of ischemic stroke in pt with hypercholestrolemia

A

Primary:
Statin if CAD or high risk of CAD

Secondary:
Statin- high dose

395
Q

Prevention of ischemic stroke in pt with DM

A

HbA1C < 7%

FBS 4-7

396
Q

Prevention of ischemic stroke in pt with smoking

A

Primary prevention:
Increases risk in a dose dependent manner

Secondary:
Smoking cessation declines risk of stroke to baseline within 2-5 years

397
Q

Prevention of ischemic stroke with physical activity

A

Dose-related benefit

398
Q

Stroke rehab

A

Dysphagia assessment, dietary modification

Communication rehab

Cognitive/psychological assessment

Exercise programs

Assessment of ambulation

Assistive devices, splints, braces

Vocational rehab

399
Q

Inv for ICH

A

General inv
+
LP (if suspect SAH but normal CT)

Cerebral angiogram (if suspect aneurism, AVM)

If typical location for hypertensive hemorrhage, repeat CT in 4-6 wko

400
Q

Tx of cerebral hemorrhage

A

Lower BP with IV meds to 140-160 systolic

ICP lowering if indicated

401
Q

The most common form of MS

A

Relapsing-remitting

402
Q

Benign MS

A

Retrospective Dx
Made after 15 years
Mild disease with no evidence of worsening (functional, MRI)

403
Q

Devic’s variant of MS

A

Neuromyelitis optica

Severe optic neuritis
+
Extensive transverse myelitis extending > 3 vertebral segments

Ab positive

404
Q

Clinically isolated syndrome

A

Single MS-like episode

May progress to MS

Early Tx with IFN may delay potential second attack

405
Q

Tumefactive MS

A

Solitary lesion > 2 cmm

Mimicking neoplasm on MRI

406
Q

Fulminant MS

A

Rapidly progressive and fatal

Severe axonal damage, inflammation and necrosis

407
Q

Pediatric MS

A

Before 18

Rare

Presentation:
Isolated optic neuritis
Isolated brainstem syndrome
Symptoms of encephalopathy

Relapsing-remitting course

408
Q

MS etiologies

A

HLA DRB1

Less sun exposure

Low Vit D levels

Certain viruses (EBV)

409
Q

Dx for RRMS

A

Dissemination in time

Dissemination in space

410
Q

Lhermitte’s sign indicates

A

Cervical cord lesion

411
Q

Uhthoff’s phenomenon

A

Worsening of symptoms in heat

412
Q

Symptoms Not commonly found in MS

A

Visual field defect

Aphasia

Apraxia

Progressive hemiparesis

413
Q

Higher disease activity of MS during its course

414
Q

Inv for MS

A

MRI:
Demyelinating plaque= hyperintense lesion on T2
Active lesions enhance with gadolinium

Dawson fingers

Cranial MRI more sensitive than spinal MRI

CSF:
Oligoclonal bands. Increased Ig G

Evoked potentials (visual/auditory/somatosensory):

Delayed but well-preserved wave forms

415
Q

Typical locations of lesions on MRI

A

Periventricular

Corpus callosum

Cerebellar peduncles

Brain stem

Juxtacortical

Dorsolateral spinal cord

416
Q

Acute Tx of MS

A

Methylprednisolone 1000/ d IV x 3-7 d

If poor response, plasma exchange

417
Q

Chronic Tx of MS

A

Disease modifying therapy:

1st line:
Teriflunomide
Interferon-B
Glatiramer acetate
BG-12

2nd line:
Natalizumab
Fingolimod

No proven efficacy for PPMS, SPMS

418
Q

Symptomatic Tx of MS

A

Spasticity:
Baclofen, dantrolene, BDZ, botulinum toxin

Bladder dysfunction:
Oxybutinin

Pain:
TCA, carbamazepine, gabapentin

Fatigue:
Amantadine, modafinil, methylphenidate

Depression:
Anti-depressant, lithium

Constipation:
High fiber intake, stool softener, laxatives

Sexual dysfunction:
Sildenafil

Education

Counseling

419
Q

Good prognostic factors for MS

A 
F
Young
Presenting with optic neuritis
Low burden on MRI
Low rate of relapse early in disease

PPMS: poor prognosis, higher disability rate, poor response to Tx

420
Q

MS med with risk of PML

A

Natalizumab

Esp if:
Positive anti-JC Ab
Lengthy treatment with natalizumab
Prior use of immunosuppresant

Med (25 decks)

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