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CM 4 GERI & NEURO > Movement and Motor Disorders > Flashcards

Movement and Motor Disorders Flashcards

1
Q

list the movement disorders

A

Essential Tremors

Huntington’s Disease

Parkinson’s

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2
Q

define movement disorders & what structre their defect arises from

A

Neurologic conditions with abnormalities in voluntary and involuntary movements in the absence of weakness.

All due to imbalance of activity in the complex basal ganglia circuits

  • Defect in basal ganglia!!
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3
Q

Hypokinetic movements

A

Akinesia – absence of movement

Bradykinesia - slowness of movement

Rigidity - ↑ tone

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4
Q

hyperkinetic movements

A

oTics

oTremor

oDystonia

oAthetosis

oChorea

oBallismus

oMyoclonus

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5
Q

compare / contrast functions of direct vs indirect pathway

and damage will result in what type of movement disorder

A

Direct Pathway - Making movements (Glutamate)

  • Substantia nigra through dopaminergic neuron to activate direct pathway and inhibit indirect pathway
  • Damage = hypokinetic

Indirect Pathway - Suppression of movements (GABA)

  • Detour to subthalamic nucleus
  • Cholinergic neurons activate indirect and suppress direct pathway
  • Damage = hyperkinetic
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6
Q

funcions of basal ganglia

A
  • Help to control movement
  • Help to regulate emotion
  • OCD: Caudate; Depression: Nucleus accumbens

•Help to regulate cognitive skills

  • Memory for skills and habits: striatum
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7
Q

define hyperkinetic movement disorders

A

characterized by involuntary movements unaccompanied by weakness and occurring in isolation or in combination.

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8
Q

how to hyperkinetic movements differ from tics

A

they cannot be suppressed by voluntary control

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9
Q

list hypokinetic and hyperkinetic movement disorders

A

Hypo - parkinsons

Hyper-

  • Essential tremor
  • Myoclonus
  • Ballismus/
  • hemiballismus
  • Chorea
  • Huntington disease
  • Athetosis
  • Dystonia
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10
Q

Rhythmic oscillation of a body part due to intermittent muscle contractions

A

Tremor

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11
Q

Sudden, brief (<100 ms), jerk-like, arrhythmic muscle twitches

A

Myoclonus

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12
Q

dance-like non-patterned involuntary movements involving distal or proximal muscle groups

A

Chorea

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13
Q

Slow, distal, writhing, involuntary movements with a propensity to affect the arms and hands (a form of dystonia with increased mobility)

A

Athetosis

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14
Q

sustained or repeated muscle contractions often associated with twisting movements and abnormal posture

A

Dystonia

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15
Q

Brief, repeated, stereotyped muscle contractions that can often be suppressed for a short time

A

tics

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16
Q

define parkinsonism

A

generic term used to define a syndrome that manifests as

  • Bradykinesia - Slowness of movement
  • Rigidity
  • And/or tremor
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17
Q

parkinsonism like dz

A

Parkinson disease (PD)

Progressive supranuclear palsy (PSP)

Multiple system atrophy (MSA)

Corticobasal degeneration (CBD)

Vascular Parkinsonism (VaP)

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18
Q

parkinson dz is caused by?

A

Sporadic/unknown – defect in dopaminergic NT

Damage to DIRECT pathway

Defect in substantia nigra

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19
Q

Braak Staging is used in what dz?

explain significance?

A

Parkinson’s starts outside of CNS!!

  • Mid stage – bradykinesia, rigidity
  • Early stage - Constipation, REM sleep disorder 10-20 yrs before onset of parkinsonian si/sx
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20
Q

RF for parkinson

A
  • Environmental (ex. rural living, well water, pesticides, herbicides)
  • Genetic (ex. LRRK2, Parkin, DJ-1, PINK-1)
  • Familial (10-15% of cases)
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21
Q

motor si/sx of parkinsons dz

A

(“TRAP”)

[Resting] tremor (“pill rolling”) in hands - characteristic

  • (also lips, chin, jaw, legs)

Rigidity (cogwheel, lead pipe)

Akinesia/bradykinesia (90%) -Most disabling symptom

Postural disturbances (stoop posture)

  • advanced si/sx
  • most common cause of falls
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22
Q

nonmotor si/sx of parkinsons

A
  • Psychiatric disorders (ex. anxiety/depression)
  • Cognitive disorders- dementia
  • REM sleep disorders – before motor sx
  • Autonomic dysfunction – orthostatic hypotension, constipation
  • Sensory dysfunction - Olfactory dysfunction, Pain, dysesthesias
  • Fatigue
  • Weight loss
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23
Q

dx criteria for parkinsosn dz

A

The presence of 2 of 3 parkinsonism features

  • Tremor
  • Rigidity
  • bradykinesia

AND good response to levodopa.

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24
Q

imaging for parkinsons dz

A
  • PET scan
  • SPECT
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25
Q

histology of parkinsons d

A

↓ of pigment in SNc –> degeneration of dopaminergic neurons

Lewy Body accumulation –> due to a synuclein

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26
Q

tx of parkinsons dz

A

Symptomatic: Levodopa/Carbidopa (Sinemet)

Dopamine agonists –

  • Pramipexole (Mirapex
  • Ropinirole (Requip)

MAO-B inhibitors

  • Selegiline
  • Rasagiline

Surgical treatment – Deep Brain Stimulation (DBS)

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27
Q

define essential tremor

etiology?

A

Rhythmic oscillation of a body part due to intermittent muscle contractions

Unknown – GABAergic dysfunction in cerebellum/cortex

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28
Q

Most common movement disorder

A

essential tremors

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29
Q

si/sx of essential tremor

A

High-frequency, bilat, symmetric, postural & action tremors that predominantly affect the UE

  • postural & action tremor - hands, head & voice.
  • Cannot write properly

The tremor is characteristically

  • improved by alcohol
  • worsened by stress
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30
Q

esstential tremors are chanracteristically

improved by____

worsened by___

A

improved by alcohol

worsened by stress

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31
Q

tx of essential tremors

first line

second line

thirs line

A

First line – BB & anticonvulsants

  • Beta blockers (Propranolol) – block peripheral non-cardiac B2 receptors in muscle spindle
  • Anticonvulsants (primidone) – block Na channel & ↑ GABA in CNS

Second line – BZD -> Inc efficiency of GABA

all fails – Botox or surgical therapies targeting the VIM nucleus of the thalamus

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32
Q

define Myoclonus

type types

A

Brief, rapid, shock-like, jerky movement arrhythmic muscle twitches consisting of single or repetitive muscle discharges.

positive myoclonus - active muscle contraction

negative myoclonus –inhibition of ongoing muscle activity

  • Asterixis – hand tremors with hand extension
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33
Q

types of myoclonus and when they occur?

A

Physiologic - Nocturnal (usually on falling asleep)

Essential - Occurs in the absence of other abnormality (benign)

Epileptic - Demonstrable cortical source

Secondary to disease process

  • Neurodegenerative eg. Wilson’s disease
  • Infectious e.g CJD, Viral encephalitis
  • Toxic e.g. penicillin, antidepressants
  • Metabolic - anoxic brain damage, hypoglycemia, hepatic failure (asterixis), renal failure, hyponatremia
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34
Q

Tx of myoclonus

A

Benzos

Valproic acid

Levetiracetam – inhibiting presynaptic Ca channel à slows down release of excitatory NT

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35
Q

define Ballismus/hemiballismus

A

Uncontrollable, poorly patterned flinging movement of an entire limb (violent chore)

  • More dramatic ballistic movements in the arms & legs.

one side of the body (Hemiballismus).

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36
Q

causes of Ballismus/hemiballismus

A

Ischemic stroke - in the contralateral subthalamic nucleus

Non-ketotic hyperglycemia – ↑ sugar –> ↓ GABA

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37
Q

tx of Ballismus/hemiballismus

A

Self-limiting - 6 to 8 weeks.

dopamine blocking/depleting agents

  • Haloperidol
  • Tetrabenazine
38
Q

define Chorea

A

“Dance”) is characterized by involuntary, irregular, purposeless, random, non-rhythmic hyperkinesias.

  • Present at rest - ↑ by activity, tension, emotional stress and self-consciousness.
  • Patient may be able to t_emporarily /partially suppress movements._
  • Disappear in sleep.
39
Q

causes of chorea

A

Drugs: Excessive dose of L-dopa, dopamine agonists, OCP, phenytoin

Inherited disorders - Huntington disease, Benign hereditary chorea, Wilson disease

Systemic disease - Thyrotoxicosis, Polycythemia vera, Toxoplasmosis in AIDS

Immune mediated - Post-strep. (Syndenham’s chorea), Lupus, Anti-PL Ab

Stroke, tumor, vascular malformation

40
Q

When treat patients for HYPOkinetic disorders with_______ can develop______ disorders

When treating pts of hyperkinetic movement disorders w/______ can develop____ like si/sx

A

When treat patients for HYPOkinetic disorders with Levodopa can develop HYPERkinetic disorders (excess dopa = choreaform)

When treating pts of hyperkinetic movement disorders w/ antipsychotics can develop parkinsonian like si/sx (hypokinetic)

41
Q

pathophys of HD

A

Huntingtin gene (­ INC CAG repeats >35) – anticipatory phenomenon

Predominantly affects the striatum.

Loss of GABAergic neurons in the striatum–> loss of GABA mediated inhibition on s_ubstantia nigra_ –> hyperactivity of dopaminergic synapses

42
Q

si/sx of HD

A

characterized by

  • motor (gait disturbances)
  • behavioral
  • oculomotor
  • cognitive dysfunction (dementia)

Athetosis/chorea

43
Q

tx of HD

A

can cause 20 Parkinsonism

  • Antipsychotics (ex. Haloperidol)
  • Tetrabenazine - dopamine depleting drugs
  • Antidepressants - Watch for suicidality

There is no adequate treatment for the cognitive or motor decline

44
Q

pathophys of Athetosis

A

The overflow is due to the failure of the striatum to s_uppress the activity of unwanted muscle groups_ —> ↑ dopaminergic activity –> inability to sustain any body part in one position

45
Q

define athetosis

A

Characterized by an inability to sustain the fingers and toes, tongue, or any other part of the body in one position

  • Sequential movement w/out your control
46
Q

pathophys of dystonia

A

Loss of inhibition at multiple levels –> ↑excitability of cortex –> abnormal recruitment of muscles not needed for specific action

47
Q

define 2 types of dystonia

A

Isolated

  • Focal - most common - cervical dystonia, blepharospasm
  • Multifocal
  • Segmental (affect two adjoining parts of the body)

Generalized : Affects most of the body–> legs & back.

48
Q

define dystonia

relieveing / aggrevating factors?

A

Sustained or intermittent muscles contractions of antagonists mm. -> abnormal, repetitive movements & posture

  • Worsened by voluntary action and associated with overflow muscle activation.
  • Relieved by relaxation, sensory tricks (Geste antagoniste)
49
Q

tx of dystonia

A

Levodopa tried in all cases of childhood-onset dystonia to test for DRD.

Anticholinergics (trihexyphenidyl)

muscle relaxers (diazepam)

GABAB receptor agonist (Baclofen)

Botulinum toxin injection – Most successful for blepharospasm, cervical and task specific dystonias.

DBS of the pallidum can provide dramatic benefits for some.

50
Q

identify anatomical regions in the brain affected by these disorders

Parkinsonism

Chronic chorea

Athetosis/dystonia

Hemiballismus

Myoclonus

Tremors

A

Parkinsonism Substantia nigra

Chronic chorea [Neo]striatum – caudate nucleus/Putamen

Athetosis/dystonia Putamen or thalamus

Hemiballismus Subthalamic nucleus

Myoclonus Cerebellar cortex/thalamus

Tremors Variable - Cerebellum/Brain stem/Frontal lobes/Thalamus

51
Q

list motor disorders

A

Tourette’s Syndrome

Guillain-Barré Syndrome

Cerebral Palsy

Multiple Sclerosis

52
Q

define pyramidal and extrapyrmidal tracts and their functions

A

Pyramidal tracts - corticobulbar & corticospinal tracts

  • Aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either
    • brainstem corticobulbar – H&N- go through the medullary pyramid
    • or spinal cord corticospinal
  • control of motor functions of the body.
  • Most common site of CVA

Extrapyramidal tracts — tracts within the spinal cord involved in involuntary movement but not part of the pyramidal tracts.

  • Subcortical region
  • functions - control of posture & muscle tone
53
Q

cc motor disorders

Corticospinal:

Corticobulbar:

Extrapyramidal:

A

Corticospinal: Muscle weakness, hypertonia, hyperreflexia, clonus, +ve Babinski’s sign.

  • Upper motor neuron lesion
  • “pyramidal signs”

Corticobulbar: Depends on the nerve affected.

  • Hypoglossal - Occur on opposite side of affected lesion

Extrapyramidal: Dyskinesias (involuntary movements)

54
Q

si/sx of Upper motor neuron lesion

A

Corticospinal

  • Muscle weakness
  • hypertonia
  • hyperreflexia
  • clonus
    • Babinski’s sign.
55
Q

pathophys of MG

A

autoantibodies directed against Ach receptors (AchR)–> ↓ available AChRs at the postsynaptic muscle membrane.

  • ACh produces small end-plate potentials –> fail to trigger muscle AP –> weakness of muscle contraction.

The amount of ACh released per impulse normally declines on repeated activity (presynaptic rundown).

56
Q

MG is due to autoantibodies against what 2 antibodies?

functions of these?

A

Anti-AchR Abs(85%)

  • ↑Turnover of AChRs
  • Damage to the PS muscle membrane
  • Blockade of the active site of the AChR

Anti-muscle-specific kinase Abs (MuSK) - ↓AchR

57
Q

si/sx of MG

A

weakness & fatigability W/O loss of reflexes or impairment of sensation)

58
Q

describe course of the si/sx of MG

A

Weakness & fatigability of skeletal muscles that worsens with exertion

  • As day goes on gets WORSE

Early MG - Cranial muscles (lids & EOM),

  • Diplopia, ptosis, facial weakness (“snarling” smile), weakness in chewing, nasal timbre speech, difficulty in swallowingà regurgitation / aspiration

Weakness becomes generalized affecting limb muscles (proximal, asymmetric)

59
Q

dx of ocular MG

A

Restricted EOM weakness for 3 years

60
Q

dx of MG

A

Antibodies to AChR, MuSK, or Ipr4 (diagnostic!!)

  • (-) does not r/o

Electrodiagnostic testing

  • Repetitive nerve stimulation – ↓ >10–15% in the amplitude.

Edrophonium test (acetylcholinesterase inhib)

  • Edrophonium (2 mg + 8 mg IV) –> improvement in muscle strength.

+/- CT/MRI: For ocular or cranial MG:

  • exclude IC lesions
61
Q

tx of MG

A

FIRST LINE- acetyl inhib + Steroids

Acetyl cholinesterase inhibitor (2-4 hrs)

  • Pyridostigmine
  • Neostigmine

Immunosuppressants

  • Systemic steroids
  • Cyclosporine A
  • Azathioprine
  • Mycophenolate mofetil
  • Cyclophosphamide – toxic metabolite

Surgical thymectomy

62
Q

define MG crisis

Tx

A

Infections or systemic disorders –> weakness –> Resp. failure–> “crisis”

Plasmapheresis

IV Immunoglobulin

63
Q

Concurrent Thymus disorder is assoc w/ what dz?

pathophys??

A

MG

Thymic disorders (ex. thymoma, thymic hyperplasia-> dysregulation of thymus –> production of autoreactive T-cells> T-cell mediated destruction of Ach receptors

64
Q

define motor and sensory tics

A

A tic is a brief, rapid, recurrent, and seemingly purposeless stereotyped motor contraction.

sensory tics, composed of unpleasant focal sensations in the face, head, or neck. (mild- severe

65
Q

types of motor tics

A

Simple, individual muscle group (blinking, twitching of the nose, jerking of the neck),

Complex, with coordinated involvement of multiple muscle groups (jumping, sniffing, head banging, and echopraxia).

Phonic tics - simple (grunting) or complex (echolalia, palilalia and coprolalia)

66
Q

tourettes syndrome is assoc w/ what other dzs?

A

assoc with anxiety, depression, ADHD, and OCD

67
Q

pathophys of toureettes

A

Not known; changes in dopamine neurotransmission, opioids, and second-messenger systems have been proposed.

68
Q

si/sx of tourettes

A

characterized by multiple motor tics & vocalizations (phonic tics).

  • characteristically can voluntarily suppress tics for short periods of time
  • but then experience an irresistible urge to express them.
69
Q

dx of tourettes

A

Diagnosed when a person exhibits both multiple motor and one or more vocal tics over the period of a year.

70
Q

tx of tourettes

A

Mild dz - Education/counseling

Habit reversal therapy

α2-adrenergic agonists: clonidine, guanfacine

Neuroleptics

  • Atypical neuroleptics (risperidone, olanzapine, ziprasidone)
  • Classical neuroleptics (haloperidol, fluphenazine, pimozide, or tiapride)

Botox- focal tics or DBS

71
Q

complication w/ tx of tourettes

A

Medication side effects (ex. tardive dyskinesia w/ classical Neuroleptics )

  • haloperidol, fluphenazine, pimozide, or tiapride)
72
Q

list classical and atypical antipsychotics

A

Atypical neuroleptics

  • risperidone
  • olanzapine
  • ziprasidone

Classical neuroleptics

  • haloperidol
  • fluphenazine
  • pimozide
  • tiapride
73
Q

define and list causes of GBS

A

Acute-onset immune-mediated demyelinating neuropathy. (more males)

acute, frequently severe, & fulminant polyradiculopathy that is autoimmune in nature

  • Antecedent Events: 1-3 wks after URI or GI
  • Campylobacter jejuni – most common cause in US
  • Mycoplasma pneumoniae
  • Recent immunizations
74
Q

pathophys of GBS

A

Demyelination –> conduction block –> flaccid paralysis & sensory disturbance –> rapid recovery w/ remyelination if axons remain intact

Severe cases : Axonal injury–> slower rate of recovery –> ↑ disability

75
Q

types of GBS

A

Acute inflammatory demyelinating polyneuropathy (AIDP) **

Acute motor axonal neuropathy (AMAN)

Acute motor sensory axonal neuropathy (AMSAN)

76
Q

si/sx of GBS

A

Rapidly evolving ascending paralysis (“rubbery legs”) (<4 wks other body parts)

  • Hyporeflexia/areflexia

Facial diparesis (~70% of pts),

  • pain in the neck, shoulder, back, or diffusely over the spine
  • Tingling dysthenias

Autonomic involvement (later) –

  • fluctuation in BP
  • postural hypotension,
  • cardiac dysrhythmias.
77
Q

dx GBS

A

recognizing the pattern of rapidly evolving paralysis with areflexia, absence of fever

CSF – albumin cytologic disassociation

  • CSF protein level (1-10 g/L) w/o ↑WBC –> pleocytosis (after 48 hrs)

Electrodiagnostic testing- Edx slowing of conduction velocity, conduction block, and temporal dispersion

  • Myelin sheath injury –> delayed conduction
  • Axonal injury – ↓ amplitude
78
Q

compare / contrast MG vs GBS

reflexes?

sensation?

A

MG - weakness & fatigability W/O loss of reflexes or impairment of sensation)

GBS - recognizing the pattern of rapidly evolving paralysis with areflexia, absence of fever

79
Q

tx of GBS

A

Treatment should be initiated ASAP

  • High dose IVIF or plasmapheresis
  • NO glucocorticoids !!!*
80
Q

causes of Cerebral palsy

A

Antenatal (80%)

  • Cerebral dysgenesis
  • Congenital infection (TORCH)
  • Substance abuse/prematurity

Intrapartum (10%) – Birth asphyxia/ trauma (breech)

Postnatal

  • Intraventricular hemorrhage/ischemia
  • Meningitis/encephalitis
  • Head trauma
  • Hyperbilirubinemia
81
Q

motor types of cerebral palse

location of brain

sx?

A

Spastic: (motor cortex) Most common (~91%)

  • Pyramidal Sx (tremors,hyporeflexia hypertonicity, tip toe walking, scissoring gait)
  • muscles are stiffer than normal.

Dyskinetic (basal ganglia)

  • Recurring, uncontrollable & i_nvoluntary movements_, exacerbated during stress
  • fluctuating tone

Ataxic (cerebellum least common)

  • Generalized hypotonia w/ loss of muscle coordination / balance
  • Wide based gait
  • ↓ proprioception
82
Q

tx of cerebral palse

A

Botox, Baclofen - control muscle spasms and seizures

Glycopyrrolate - control drooling

Pamidronate -may help with osteoporosis

83
Q

define MS

A

Autoimmune (T-cell mediated destruction of myelin sheath proteins) - characterized by chronic inflammation, demyelination, gliosis, & neuronal loss

Demyelination - pathological hallmark and evidence of myelin degeneration is found at the earliest time points of tissue injury.

84
Q

list types of MS

A

Relapsing Remitting Disease (RMS): ~85% - progression characterized by relapses of active disease with complete recovering during periods of remission.

Secondary Progressive Disease (SPMS): R&R then becomes progressive

Primary progressive disease (PPMS): ~15% - symptoms are progressive from the onset NO remission!

85
Q

patho of MS

A
  • BBB problem –> T-cells get inside CNS & get activated –>
  • T-cell mediated destruction of myelin proteins & cytokine production –> inflammation
  • B-cells produce abs against myelin sheath –> complement activation & abs mediated phagocytosis
86
Q

RF for MS

A
  • Genetic predisposition
  • Vit D deficiency
  • EBV exposure in early childhood
  • Smoking
87
Q

si/sx of MS

A

Sensory, motor &autonomic

Sensory symptoms:

  • paresthesia’s (e.g., tingling, prickling sensations, “pins and needles,”
  • painful burning) and hypesthesia (e.g., reduced sensation, numbness,
  • or a “dead” feeling).

Optic neuritis (ON) – common early sx

  • diminished visual acuity, dimness,
  • decreased color perception (desaturation) in the central field

Weakness of the limbs. Exercise-induced weakness is a characteristic symptom of MS.

88
Q

dx of MS

A

At least 2 episodes of Sx that occur at different points in time

MRI (focal white matter lesions)

Lumbar Puncture – mild pleocytosis and a total protein usually normal.

  • Protein > 100mg/dl is unusual and should be evidence against MS

Evoked potentials - detect slow or abnormal conduction in response to visual or auditory stimuli

89
Q

tx of acute attacks of MS

A

IV Glucocorticoid – methylprednisolone

90
Q

Disease modifying therapies of MS

highly effective

modestly effective

A

Highly Effective:

  • Dimethyl fumarate – anti-inflammatory effects
  • Natalizumab - preventing lymphocytes from penetrating the BBB and entering the CNS
  • Alemtuzumab – lymphocyte (B & T) depletion

Modestly Effective:

  • Interferon β - ↓MHC Class II, ↓T cell proliferation
91
Q

symptomatic tx of MS

Spasticity –

Optic Neuritis

Fatigue –

Pain –

Tremor –

A

Spasticity – Baclofen, Cyclobenzaprine

Optic Neuritis – Methylprednisolone, Oral Corticosteroids

Fatigue – Amantadine, Anti-depressants

Pain – Gabapentin, Pregabalin

Tremor – Propranolol, Primidone

92
Q

motor disorders are due to defect in ??

movement disorders are due to defect in??

A

motor disorders are due to defect in- pyrmidal/ extrapyrimidal tracts

movement disorders are due to defect in- basal ganglia

CM 4 GERI & NEURO (4 decks)

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