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Neuro diseases Flashcards

1
Q

What is the most common NMJ disorder? It’s a ____ disorder characterized by _____

A

Myesthenia gravis
Autoimmune
General muscle weakness

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2
Q

Main subtype of GBS in NA

A

Acute inflammatory demyelinated polyneuropathy

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3
Q

Describe the pattern of paralysis in GBS

A

Acute ascending flaccid paralysis

lower –> upper limbs

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4
Q

Mechanism of autoimmunity in GBS?

A

Molecular mimicry (–> T cells –> B cells –> Abs –> macrophages)

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5
Q

Demyelination in GBS is ___

A

Segmental

Schwann cells remyelinating at first

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6
Q

Damage to ___ nerve can cause respiratory failure/death in GBS

A

Phrenic nerve

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7
Q

3 diagnostic tests in GBS

A

Lumbar puncture
NCV/EMG
PFTs

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8
Q

What will NCV/EMG show in GBS

A

reduced/blocked NCV

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9
Q

What will CSF show in GBS

A

Albuminocytologic dissociation

High protein/albumin without high WBCs

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10
Q

Treatment for GBS

A

supportive + pain management
IVIg & plasmapheresis can help speed recovery but don’t impact prognosis
STEROIDS DON’T HELP IGs are already floating around

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11
Q

Nadir of GBS usually reached within ___

A

1 month

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12
Q

Carpal tunnel syndrome involves compression of the __ nerve

A

Median

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13
Q

in carpal tunnel syndrome what are the main symptoms/sensations and where

A

pain, numbness, tingling (starts as dull ache)
of thumb, index, middle finger, ring finger on lateral side
Also muscle weakness/clumsiness

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14
Q

What makes up the roof of the carpal tunnel?

A

Transverse carpal ligament = flexor retinaculum

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15
Q

How many nerve are within the carpal tunnel?

A

Only one (median)

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16
Q

What atrophy can be seen in carpal tunnel

A

Thenar muscle (recurrent branch of median nerve)

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17
Q

Why is the sensation at the central base of palm unaffected in peripheral neuropathy

A

Palmar branch of median nerve is unaffected because branches off upstream of carpal tunnel

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18
Q

5 treatments for carpal tunnel

A 
Behaviour modification/ergonomics
Physical therapy
Splinting
Corticosteroids
Surgical division of transverse carpal ligament
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19
Q

Name 4 patterns of MS progression

A

1) Relapsing-remitting (90% @ diagnosis)
2) Secondary progressive (50% become this)
3) Primary progressive
4) Progressive-relapsing

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20
Q

Most often earliest manifestation of MS = ____; can cause what defect that can be seen on physical exam?

A 
Optic neuritis (inflammatory demyelination of optic nerve)
Relative afferent pupillary defect
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21
Q

What is Lhermitte sign?

A

Shooting electric sensation travelling down spine when you flex neck
Seen in demyelinating diseases like MS

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22
Q

Cerebellar involvement in MS leads to what pattern of symptoms?

A

Charcot neurological traid: Disarthria/scanning speech, Nystagmus, Intention tremor

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23
Q

1st choice test for MS

What do you see?

A

MRI of brain + spine with/without Gado

Shows white matter PLAQUES

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24
Q

Gado enhances active lesions up to ____ after attack

A

6 weeks

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25
Q

Other than MRI, what diagnostics can be done for MS? (2)

A

1) Visual evoked potentials (EEG) - slowed optic nerve conduction
2) CSF (lymphocytic pleocytosis, oligoclonal bands (intrathecal IgG synth), myelin basic protein

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26
Q

Summarize the McDonald Criteria for MS diagnosis

A

1) Dissemination in time: 2+ attackes 30+ days apart (or MRI showing enhancing + non-enhancin lesions, or CSF oligoclonal bands)
2) Dissemination in space: lesions in 2+ diff regions of CNS confirmed by objective diagnostic findings

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27
Q

Treatment of acute MS exacerbation

A

High-dose IV glucocorticoids
2nd line: phalsmapheresis
Other options: ACTH gel (if corticosteroids don’t work), IVIg, cyclophosphamide

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28
Q

What is a disease-modifying MS drug that suppresses T cell activity and can be used to prevent exacerbations in all types of MS? Rom?

A

Interferon beta

SubQ

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29
Q

What is acute transverse myelitis? Most common cause?

A

Acute inflammation of grey/white matter in 1+ adjacent spinal cord segment (usually thoracic)
MS = most common cause
(others include vasculitis, SLE, anti-PL syndrome, other autoimmune disorders/infections)

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30
Q

Testing for acute transverse myelitis

A

MRI (spine) for cord swelling, r/o
CSF analysis
Brain MRI for plaques (MS)
Testing for various causes

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31
Q

Acute transverse myelitis is diff that GBS how?

A

GBS doesn’t locate to a specific spinal segment! ATM has SEGMENTAL deficits

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32
Q

Prognosis of Acute Transverse Myelitis

A

1/3 recover, 1/3 have lasting weakness/urinary urgency, 1/3 bedbound + incontinent

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33
Q

Mydriasis vs miosis

A 
Mydriasis = fixed or excessive pupil dilation
Miosis = excessive contriction
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34
Q

What are the 3 “types” of pain

A
  1. Nociceptive (direct or indirect (inflamm))
  2. Neuropathic pain (peripheral or central nerve damage)
  3. Centralized pain (no stimulus)
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35
Q

Sensory nerve fibre types from largest/fastest to smallest/slowest! (5)

A 
A alpha (proprioception)
A beta (touch/pressure)
A delta (pain/temp)
B (visceral afferents, autonomic preganglionics)
C (pain, temp, autonomic postganglionics)
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36
Q

Which nerve fibre type is unmyelinated?

A

C

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37
Q

Spinothalamic tract carries ___ signals and is part of the ___ pathway

A

Pain & temp

Anterolateral

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38
Q

Spinal lesions:
A lesion of GREY matter will affect ____
A lesion of WHITE matter affects ____
(what levels/sides)

A

GREY –> at that spinal level only, ipsilaterally (dematome/myotome)
WHITE –> sensory and/or motor BELOW, side depends on location of crossing

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39
Q

CN V = ? VII = ?

Crosses over where?

A

Trigeminal, facial

Pons

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40
Q

unique location where a large number of motor and sensory fibers travel to and from the cortex

A

Internal capsule

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41
Q

Headaches: 4 EMERGENT + 4 URGENT red flags

A

Emergent: thunderclap, fever/meningismus, papilledema w/ focal signs or lowered LOC, acute glaucoma
Urgent: temporal arteritis, papilledema w/out above, relevant systemic illness, new headache w/ cognitive change in elderly patient

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42
Q

What is a coup-countrecoup injury

A

Concussion injury where injury occurs on the 2 opposite sides

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43
Q

Concussion is a subset of ___

A

mTBI

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44
Q

Severity of TBI is classified using what? What would mild be?

A

GCS

Mild = 13-15

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45
Q

Most common neurodegenerative etiology of dementia? Most common non-neurodegenerative etiology?

A 
Alzheimers (>50% of dementia)
Cerebrovascular disease (20%)
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46
Q

Define aphasia and paraphasia

A

Aphasia = impairment of communication/understanding of speech and/or writing
Paraphasia can occur in aphasia, and is producing unintended words/sounds (e.g. saying “hat” instead of “bat” = phonemic paraphasia, saying “week” instead of “month” = semantic paraphasia)

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47
Q

What is the DSM-5 criteria for dementia?

A

Significant decline in cognition (learning/memory, language, executive fn, attention, perceptual-motor and/or social)

  • INTERFERES w/ daily life
  • NOT exclusively during delirium or explained by another disorder
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48
Q

The mini-mental state examination (MMSE) includes what domains? (6)
Cutoff score for dementia?

A

1) Orientation
2) Registration (immediate memory)
3) Attention/calculation
4) Recall (STM)
5) Language (speaking/understanding)
6) Copying a picture (visuospatial)
<25/30 = dementia

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49
Q

What test is often added to the MMSE? What other assessment tool has this? What is one component it has that the MMSE doesn’t which is often ADDED to the MMSE? Cutoff for dementia?

A

Clock-drawing test (spatial + abstract thinking)
Montreal cognitive assessment (MOCA)
- abstraction (finding similarities b/w things)

Cutoff = 25/30

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50
Q

Important lab tests in all pts presenting with dementia-like symptoms

A

B12 deficiency, hypothyroidism

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51
Q

Lab markers for B12 and folate deficiency

A

High homocysteine in both

High methylmalonic acid only in B12

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52
Q

Imagine in patients presenting with potential dementia

A

Noncontrast CT or MRI

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53
Q

Dementia AKA

A

Major neurocognitive disorder

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54
Q

In vascular dementia what might you see on brain imaging?

A

Lacunar infarcts (subcortical stroke)

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55
Q

What binds the NDMA receptor?

A

Glutamate

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56
Q

3 modalities of treatment for dementia

A

1) Memory training
2) Cholinesterase inhibitors
3) Mementine

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57
Q

___substances should be avoided in dementia as they may lead to further deterioration in cognitive funcitoning

A

Anticholinergic

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58
Q

Examples of cholinesterase inhibitors that can be prescribed for Alzheimers/dementia
When are they contraindicated?

A

Dona Riva dances at the nursing home Gala: Donepezil, Rivastigmine, Galantamine

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59
Q

How does memantine work for dementia? ADEs? Indications?

A

NDMA-receptor antagonist, reduces glutamate-induced Ca-mediated excitotoxicity
Mod-advanced Alzheimers, vascular dementia
ADEs impact CNS (headache, dizziness, confusion, seizures, etc)

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60
Q

What is Wernike encephalopathy caused by? Classic triad

A

Thiamine deficiency

Confusion + ataxia + opthalmoplegia

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61
Q

3 distinct features of Lewy Body Dementia

A

Visual hallucinations
Parkinsonism
Attention impairment

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62
Q

In pseudodementia, cognitive deficits are associated with ____ and usually improve after ____

A

Major depression

Antidepressant therapy

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63
Q

What subset of dementia is associated with early changes in personality/apathy

A

Frontodemoral dementia (behavioural variant, most common)

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64
Q

What type of dementia often present with asymmetric/focal deficits (e.g. hemiparesis),

A

Vascular dementia (lacunar infarcts common)

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65
Q

Prognosis of Alzheimer disease & causes of death

A

3-10 year survival post-diagnosis

Infections (difficulty swallowing–> pneumonia), dehydration, malnutrition, falls

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66
Q

Pathophys of Alzheimers

A

1) Amyloid beta plaques (extracellular in grey matter)
2) Neurofibrillary tangles (intracellular hyperphosphorylated tau protein, neurotoxic)
3) Cholinergic neuron degeneration –> ACh deficiency

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67
Q

Define adaptive functioning

A

Ability to handle common life demands, independence compared to others of age/background

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68
Q

Global developmental delay

A

Significant delay in 2+ major developmental domains in children <5yo

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69
Q

Diagnostic criteria for intellectual disability

A

Impaired intellectual + adaptive functioning in at least one of the following domains:

1) Conceptual (incld language, math, memory, judgement)
2) Social
3) Practical (ADLs)

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70
Q

Neurodevelopmental disorders (12) are divided into what 6 categories in DSM-5?

A
  1. ASD
  2. ADHD
  3. Specific learning disorder
  4. Intellectual disabilities (ID & GDD)
  5. Communication disorders
  6. Motor disorders
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71
Q

4 key features of ASD

A
  1. Deficits in social-emotional reciprocity
  2. Deficits in nonverbal communication
  3. Difficulty developing, maintaining, understanding social relationships
  4. Restrictive/repetitive behaviours and/or hypo-hyper-reactivity to specific sensory stimuli
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72
Q

ADHD involves what 2 categories of behaviours

A

Inattention

Hyperactivity & impulsivity

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73
Q

Dyslexia is a form of ___ disorder

A

Specific learning disorder

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74
Q

ID is classified as what on an IQ test?

A

At least 2 SD below mean (<70 if mean 100, SD = 15)

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75
Q

Stuttering is what disorder?

A

Childhood-onset fluency disorder (type of communication disorder)

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76
Q

What class of drug is used for Tic disorders when non-medical interventions are exhausted?

A

Antidopaminergic drugs (tetrabenazine, fluphenazine, risperidone)

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77
Q

Common ADHD drugs (2)

A

Methylphenidate (Ritalin)

Amphetamines (e.g. Adderall)

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78
Q

What is the mutation in fragile X syndrome?

A

Trinucleotide repeat (CGG) in UTR of FMR1 on X chromosome (encodes FMRP)

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79
Q

Why does trinucleotide repeat expansion prevent transcription of FMRP?

A

The cytosines are methylated –> promoter not accessible

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80
Q

What is “anticipation” in genetics?

A

Conditions becomes more severe w/ successive generations

Common in trinucleotide repeat expansion disorders, which can expand more and more with each generation

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81
Q

Characteristic physical features of Fragile X syndrome

A

Long narrow face w/ prominent jaw/forehead
Large ears, face, testes
Pes planus, hypermobility, mitral valve prolapse (CT weakness)

82
Q

Cognitive/motor impacts of fragile X?

A

ID
Delayed speech & motor development
Hyperactivity, autistic behaviour

83
Q

Disorders associated w/ fragile X? (3)

A

ASD
ADHD
Epilepsy

84
Q

Can females have symptoms of Fragile X syndrome?

A

Yes but generally more mild, depends on pattern of X chromosome inactivation

85
Q

What are premutation carriers in Fragile X?

A

have 55-200 repeats –> mild symptoms, full mutation is >200 (up to 44 is normal)

86
Q

Diagnosis of Fragile X is by…

A

DNA test

87
Q

Premutation carriers of fragile X can present with what 2 related disorders?

A

1) Fragile X-associated Tremor Ataxia Syndrome (FXTAS) - adult-onset tremor, ataxia, cognitive/memory issues
2) FMR1-related POI

88
Q

By what age should a child stand/walk alone

A

12 months

89
Q

By what age should a child run

A

18 months

90
Q

By what age should a child sit w/out support

A

6 mo

91
Q

By what age should a child say mama/dada indiscriminately?

A

9 mo

92
Q

Disease with hyperorality memory loss, emotional changes, insatiable appetite, extreme sexual behaviour, indifference

A

Kluver-Bucy syndrome

lesions affecting bilateral temporal lobes, especially the hippocampus and amygdala

93
Q

The locus coeruleus is part of the ___ in the ____ and produces____

A

RAS
Pons
Norepinephrine

94
Q

The Raphe nucleus in the midbrain produces

A

Serotonin

95
Q

The ventral tegmentum in the midbrain has ___ neurons

A

Dopaminergic

96
Q

Nucleus accumbens is part of the ___ and is part of the _____. How so?

A

Basal ganglia
Reward circuit
Dopamine from VTA –> desire + motivation
Serotonin from raphe nuclei –> inhibition

97
Q

Name the blood vessels affected in epidural, subdural, and subarachnoid hematomas

A

Epidural: meningeal vessels
Subdural: bridging veins
Subarachnoid: cerebral arteries, usually in circle of willis (usually s/2 aneurysm)

98
Q

Acute hemorrhages appear ___ on noncontrast CT

A

Hyperdense (bright)

99
Q

Which cranial hemorrhage type appears lens-shaped? Crescent-shaped?

A 
Epidural = lense (sutures)
Subdural = crescent
100
Q

Pia mater extends as ___ from conus medularis –> coccyx

Clinical relevance?

A

Filum terminale

Where you do LPs (not enough space in the subarachnoid space where the SC runs)

101
Q

Passage of CSF through ventricles

A

Lateral ventricles –> interventricular foramina (of Monro) –> 3rd ventricle –> cerebral aqueduct –> 4th ventricle –> central canal

102
Q

Choroid plexus is where? What cell type produces CSF?

A

Lateral, 3rd, and 4th ventricles

Ependymal cells

103
Q

CSF drains from subarachnoid space into ____ via ____

A 
Superior sagittal sinus 
Arachnoid villi (granulations)
104
Q

CSF enters subarachnoid space via? (3)

A 
Lateral apertures (foramen of Luschka) x 2
Median aperture (foramen of Magendie)
105
Q

Broca’s area (location & function)

A 
L frontal (usually)
Speech production
106
Q

Wenicke’s area (location & function)

A 
L temporal  (usually)
Speech comprehension
107
Q

2 main watershed areas in the brain

A

ACA-MCA

MCA-PCA

108
Q

New definition of TIA

A

Temporary, focal ischemia causing neurological deficits
NO infarction
NO permanent LoF

109
Q

Most common sites of atherosclerosis in the brain?

A

Branching points, esp internal carotid & MCA

110
Q

What is a paradoxical embolism

A

Clot moves from vein –> artery without getting lodged in pulmonary circulation because of an ASD or other defect

111
Q

What is a lacunar stroke?

A

A noncortical infarct (of the small penetrating arteries supplying internal capsule, BG, pons, thalamus), and thus lacks cortical signs (no aphasia, hemianopsia, agnosia, apraxis)

112
Q

2 tissue zones in a stroke

A 
Ischemic core (tissue dies)
Ischemic penumbra (preserved by collateral circ, may survive if quick action taken)
113
Q

_____is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while ____is characterized by cell swelling caused by intracellular accumulation of fluid.

A

Vasogenic edema

Cytotoxic edema

114
Q

How can stroke lead to herniation?

A

Inflammation disrupts BBB –> vasogenic edema –> mass effects

115
Q

What is the FAST acronym for stroke

A

Facial drooping
Arm weakness
Speech difficulties (aphasia, dysarthria)
Time!!

116
Q

How is FLAIR MRI diff than T2-weighted?

A

Similar in that grey matter is brighter than white, but different because it removes signal from CSF

117
Q

T1 vs T2 MRI

A

T1 –> FAT is bright, white matter brighter than grey

T2 —> Fat & WATER is bright (so CSF shows up), white matter darker than grey

118
Q

For both ischemic & hemorrhagic strokes, ___ is the most important nonmodifiable RF & ____ is the most important modifiable RF!

A

Age

Arterial hypertension

119
Q

2o prevention options after stroke

A 
Antiplatelet therapy (aspirin, clopidogrel)
Manage RFs (hypertension, AFib, DM, lipids, thrombophilia)
120
Q

Initial drug used for status epilepticus

A

Benzodiazepines: lorazepam, diazepam, midazolam

121
Q

Name 5 common seizure drugs

A 
Lamotrigine
Valproate
Carbamazapine
Phenobarbital (children)
Topiramate
122
Q

Define status epilepticus

A

> 5 min continuous or >2 seizures w/out regaining full consciousness interictally

123
Q

Min temp for febrile seizure

A

38C

124
Q

What are 3 factors that make febrile seizure “complex” (only need at least 1)

A

> 15 min
Focal
1 in 24 hours

125
Q

Normal CSF pressure is less than

A

200 mm H2O

126
Q

2 bacteria and 3 viruses that most cause meningitis?

A 
Neisseria meningitidis (meningococcal), Streptococcus pneumoniae
Herpes simplex, HIV, enteroviruses
127
Q

What pathogen might cause meningitis at birth

A

Maternal Group B Strep

128
Q

Classic triad of meningitis?

A

Headaches
Fever
Nuchal rigidity
(only 50% present with full triad!)

129
Q

Indications for imaging before LP (suspected meningitis)

A 
LP FAILS:
Focal neuro deficits
Altered mental status
Immunocompromised, Intracranial hypertension 
Lesions (in brain)
Seizures (doesn't apply to children)
130
Q

Non-blanching rash in suspected meningitis raises suspicion of

A

Meningococcal meningitis (Neisseria meningitidis)

131
Q

Prevention of meningitis?

A

Vaccines: meningococcal, Hib

132
Q

Which pathogens causing meningitis require postexposure prophylaxis for contacts?

A

N meningitidis

H influenzae

133
Q

Empiric AB therapy for meningitis

A

Vancomycin
Ceftriazone
+ampicillin if Listeria risk (old, newborn, pregnant, immunocomp)
+Dexamethasone before/concurrently to reduce inflamm

134
Q

Acyclovir should be used for what types of encephalitis

A

HSV

VZV

135
Q

Atrophy vs dystrophy

A 
Atrophy = reduction in SIZE of muscle fibres
Dystrophy = reduction in NUMBER Of muscle fibres
136
Q

Typically, proximal weakness = ___, distal = ____

A 
Proximal = muscle
Distal = nerve
137
Q

General pathophys of myasthenia gravis

A

Autoantibodies against postsynaptic nicotinic ACh receptor (thymus involved)

138
Q

Diagnosis of myasthenia gravis

A

AChR Ab
EMG showing decreased response after repetitive nerve stimulation
(do a chest CT to r/o thymoma)
Other tests like Simpson test (looking upward 1 min), ice test (improvement)

139
Q

First line treatment for myasthenia gravis

A

Cholinesterase inhibitors: Pyridostigmine

140
Q

If pt suddenly deteriorates after responding well to treatment, they might have what going on? Features?

A 
Cholinergic crisis (affects both NAChRs & MAChRs)
SLUDGE: salivation, lacrimation, urination, defecation, GI disturbances, emesis
Also fasiculations, tachycardia
141
Q

What can trigger myasthenic crisis? Treatment?

A

Infection, surgery/anesthetics, pregnancy, meds

Treatment: IVIg, plasmapheresis, intubation

142
Q

Basic pathophys of BMD/DMD

A

Mutation of dystrophin gene on X chromosome
Frameshift/nonsense –> DMD
Missense/inframe deletion –> BMD
Messed up dystrophin –> muscle cell necrosis, replaced w/ CT & fat (pseudohypertophy, weakness)

143
Q

What sign is characteristic of DMD?

A

Gower maneuver (walking up thighs using hands)

144
Q

Heart complication of DMD?

A

Dilated cardiomyopathy

Arrhythmias

145
Q

Gait characteristic of DMD?

A 
Duchenne limp (waddling) 
Bilateral Trendelenburg compensated w/ curved upper body
146
Q

Toe-walking in DMD caused by?

A

Contracture/shortening of heel chords

Can be seen earlier as a compensation for hyperlordosis & weakness of hip flexors

147
Q

Diagnosis of DMD

A

High CK, aldolase

Genetic analysis –> dystrophin gene mutation

148
Q

Treatment for DMD

A 
Not great :(
Glucocorticoids
ACEi/BB to slow dilated cardiomyopathy
Supportive therapy, surgeries for contracture/scoliosis
Exon-skipping therapies
149
Q

Describe a positive Rinne test

A

Air > bone

150
Q

decibel level where 50% correct signals

A

Auditory threshold

151
Q

What is otosclerosis?

A

Overgrowth of stapes footplate –> fixation of bone

152
Q

What is cholesteatoma?

A

Chronic otitis media

Keratinizing squamous epithelium grows from tympanic membrane into middle ear mucosa –> inflamm, can destroy middle ear

153
Q

What is the Meniere disease? What is the Meniere triad?

A

Endolymph hydrops (impaired resorption)

1) Peripheral vertigo
2) Fluctuating unilateral SNHL
3) Unilateral tinnitus

154
Q

In what type of hearing loss is it easier to hear in noisy environments?

A

Conductive

155
Q

What is the most common cause of SNHL?

A

Presbycusis (age-related progressive damage to hair cells in organ of Corti esp at narrow/stiff basal end)

156
Q

What are the TORCH infections

A 
Toxoplasmosis
Others (syphilis, varicells, parvovirus B19, listeriosis)
Rubella
Cytomegalovirus
Herpes Simplex Virus
157
Q

What is glue ear

A

Chronic OM w/ effusion

ETD (esp after acute OM) –> neg middle ear pressure –> transudate builds up and can’t drain

158
Q

5yo is old enough to undergo what general type of hearing testing

A

Pure tone audiometry

159
Q

Inheritance of neurofibromatosis

A

Autosomal dominant inheritance (or spontaneous mutation)

160
Q

What is a neurofibroma?

A

Benign nerve sheath tumor originated from neural crest cells

Affects myelinated nerves

161
Q

Common types of tumors in Neurofibromatosis Type 2

Another common symptoms

A

Vestibular schwannomas (acoustic neuromas)
Cerebral/spinal tumors: meningiomas, ependymomas)
Neurofibromas not actually as common?

Early-onset cataracts

162
Q

What is an acoustic neuroma? AKA?

A

AKA Vestibular Shwannoma
Benign tumor arising from Schwann cells in CNVIII within internal acoustic meatus
(usually unilateral, bilateral suggestions neurofibromatosis Type 2)

163
Q

What nerve other than CN VIII moves through the internal acoustic meatus?

A

CN VII (facial)

164
Q

Is horizontal or vertical nystagmus more alarming?

A

Vertical (more indicative of potential central cause)

165
Q

Central vs peripheral nausea: which has worse nausea? Which worse imbalance? Which more motion-sensitive?

A

Central –> worse imbalance
Peripheral –> worse nausea
Peripheral –> more motion-sensitive

166
Q

3 requirements of brain death

A

1) Coma w/ identified cause
2) Absence of brainstem reflexes
3) Apnea
(**before apnea testing make sure temp high enough, BP high, no chemical disturbances/drugs that could confound)

167
Q

Fundamental pathophys of parkinson’s

A

Degeneration of dopaminergic neurons in the substantia nigra

Lewy body formation

168
Q

Decreases in ACh synthesis by nucleus basalis of Meynert are associated with __ and ___ diseases. Increases associated with ___ disease

A

Decreases: Alzheimer, Huntington
Increases: Parkinson

169
Q

The earliest prodrome sign of parkinson’s is often what? Why?

A

Constipation (early Lewy Body formation at intestinal autonomic neurons)

170
Q

Parkinsonism triad

A

Bradykinesia + rigidity + resting tremot

171
Q

Describe a parkinsonian gait

What are fenistation, propulsion, and freezing?

A

Shuffling, small steps
Fenistation = increasingly quick steps
Freezing = can’t start/continue movement
Propulsion = forward-leaning

172
Q

In parkinson’s do motor symptoms usually begin uniliaterally or bilaterally?

A

Unilaterally

173
Q

Name 6 drug categories for parkinson’s

A

1) L-DOPA (dopamine precursor that can cross BBB)
2) Carbidopa (reduces peripheral conversion of L-DOPA –> dopamine)
3) COMT inhibitors (reduce central/peripheral dop metabolization)
4) MAO-B inhibs (reduce central dop metab)
5) Dopamine agonists
6) Anticholinergic drugs
7) NMDA antagonists

174
Q

___ is the most affective drug for motor symptoms of parkinsons, but leads to unavoidable ____. Strategy to reduce this?

A

L-DOPA
Unavoidable motor fluctuations (hypokinesia, dyskinesia)
Take really frequently throughout the day

175
Q

Don’t prescribe L-DOPA if you have ____

A

Glaucoma (increases intraocular pressure)

176
Q

Example of NMDA antagonist used in parkinson’s

A

Amantadine

177
Q

Carbidopa inhibits what enzyme?

A

Dopamine decarboxylase

178
Q

Inheritance of huntington disease

A

Autosomal dominant inheritence

CAG repeats in huntingtin gene, inherited w/ ANTICIPATION

179
Q

How are GABA, ACh, and dopamine affected in Huntington?

A

Less GABA
Less ACh
More dopamine

180
Q

Neuronal degeneration/gliosis occurs where in huntington?

A

Striatum (but then progresses to thalamus, cortex)

181
Q

Motor symptoms in Huntington’s might change how as the disease progresses?

A

Start hyperkinetic/choreatic movements (indirect pathway affected)
Both pathways affected –> overall DECREASE of excitatory thalamic transmission to cortex –> HyPOkinetic/akinetic symptoms

182
Q

ALS generally starts with what symptoms (though presentation is variable)

A

Asymmetric weakness in hands/feet

183
Q

What is sensory gait

A

Loss of proprioceptive input (uncontrolled diabetes, B12 deficiency)
–> stomping gait (esp in dark)

184
Q

What is ataxic gait

A

Wide-based, clumsy/staggering (like drunk)
Cerebellar disease
Titubation when standing (swaying around) - occurs with eyes open unlike Romberg

185
Q

Characteristics of hemiplegic gait (after stroke)

A

Flexor hypertonia of upper limb, extensor hypertonia of lower limb
Foot drop
Circumduction of food
Loss of normal arm swing

186
Q

“Shock-like movements” =

A

myoclonus

187
Q

Jerking movements that randomly move around diff parts of body =

A

Chorea

188
Q

How to distinguish postural tremor (i.e. essential tremor) from true resting trmoe

A

How rapidly it manifests after new posture assumed (immediate for postural, delayed for rested = “resetting” or “reemergence”)

189
Q

Abnormal characteristic postures/movements, produced by slow/sustained muscle contraction distorting limbs, trunk, neck, face, mouth

A

Dystonia

190
Q

Define corticobulbar tract

A

Motor pathway from motor cortex to motor nuclei of CNs in brainstem

191
Q

Affect of UMN lesion on reflexes

A

Acute atonia/hyporeflexia (spinal shock)

FOLLOWED by the hyperreflexia/spasticity

192
Q

Upgoing plantar response occurs in a ____motor neuron lesion

A

Upper

193
Q

How do you differentiate UMN and LMN lesions of facial nerve?

A

UMN lesion –> paralysis only in lower half of face (upper half has ipsi + contralateral UMN innervation, redundancy)
LMN would affect full side of face

194
Q

___ supplies brain regions for lower limbs, ___ supplies hand/face

A

ACA lower limbs

MCA hand/face

195
Q

The oculomotor nerve (CN III) controls all eye movement muscles except ___ and ____
What else does it control?

A

Except lateral rectus (CN VI) & superior oblique (CN IV)

Also levitator palpebrae (eyelid) + pupillary constrictors (parasymp division)

196
Q

Why are anterior and posterior spinal cord affected differently by spinal artery infarcts?

A

Only 1 anterior spinal artery –> bilateral impacts of infarction
2 posterior spinal arteries –> only affected on 1 side

197
Q

EMG/NCV signs for demyelination and axonal loss?

A

Demyelination –> slowed CV

Axonal loss –> reduced amplitude of CMAP/SNAP

198
Q

What process has to occur before repair when axonal contents damaged?

A

Wallerian degeneration

199
Q

B12 deficiency can cause what severe neuropathy?

A

Subacute combined degeneration (loss of dorsal columns/corticospinal tracts –> hyperreflexia, loss of proprioception/vib sensation)

200
Q

painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas

A

Mononeuritis multiplex (multiple mononeuropathies)

201
Q

What is the most common cause of peripheral neuropathy? General presentation?

A

Diabetes
Usually DSPN (distal (length-dependent) symmetric sensorimotor polyneuropathy)
Mixed demyelinating & axonal

Preclerkship (25 decks)

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