Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro 3 (mine) > Movement Disorders CPC & Examination of Coordination and Gait > Flashcards

Movement Disorders CPC & Examination of Coordination and Gait Flashcards

1
Q

Describe the “Extrapyramidal signs” that accompany disorders of the
cerebellum and basal ganglia. How do these differ from “pyramidal”
dysfunction?

A

Extrapyramidal signs: abnormal movement, posture, or muscular tone, NOT paresis or sensory loss.

Basal Ganglia Disorders:

  • tremor (usually resting)
  • hypokinetic (rigidity, bradykinesia)
  • hyperkinetic (chorea, athetosis, akathisia, dystonia–contrac of ag/antag muscles resulting in fixed, painful, abnormal postures)
Cerbellar Disorders:
Synergy (ataxia): (dymetria--past-pointing/overshoot--test w/ finger nose finger and heel shin test, dysdiadochokinesia--impaired rapid alternating movement, decomposition of movement)
-Equilibrium (dysequilibrium)
-tone (hypotonia)
-tremor (usually action)
-nystagmus

Other tests:

  • pronator drift (pyramidal tract dysfun, parietal lobe dysfunc, cerebellar disease–ipsilateral)
  • Speech (Lalala CN12; Papapa CN7;KaKaKa CN10)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Distinguish among primary clinical features of dementing diseases and
movement disorders

A

f

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the key histologic hallmarks of the “synucleinopathies”

A

f

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Romberg test

A
  • tests station/gait
  • feet together, eyes closed–>positive with unsteadiness
  • pull test–>examiner pulls on pt’s shoulders–>step back=positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Testing gait

A
  • casual gait
  • forced gait (walk on heels, toes, ankles inverted)
  • tandem gait (heel to toe): pts w/ truncal ataxia (damaged cerebellar vermis or assoc pathways) will have difficulty esp.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cerebellar lesion signs

A 
HANDS Tremor
Hypotonia
Ataxia/Asynergia (3 Ds)
Nystagmus
Dysarthria
Stance and gait
Tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Examination of tone

A

(motor exam)
look for:
-rigidity (steady heightened muscular tension present in opposing muscle groups–lead pipe or cogwheel feeling)

  • spasticity–velocity dependent increase in tension with passive lengthening
  • gegenhalten or paratonia: pt seems to oppose any passive motion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examination of coord

A 
sppech rapid alt movements
hands rapid alt movements
precision hand movements
foot rapid alt movements
rebound
check reflex
FNF
Heel:shin-->toes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What could a positive Rhomberg mean?

A
  • impaired proprioception (DC/Spinal cord)
  • Impaired vestibular function (fall toward lesion)
  • impaired cerebellum func (mainly vermis or vestibulocerebellum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hemiparetic gait

A

-unilateral UMN injury
-on affected side: arm flexion, adduction, internal rotation
-lower extremity in extension with plantar flexion of the foot
and toes
-When walking, the patient will hold his or her arm to one side and drags
his or her affected leg in a semicircle (circumduction) due to weakness of distal
muscles (foot drop) and extensor hypertonia in lower limb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diplegic gait

A
  • spasticity in LE>UE
  • NARROW base
  • drag both legs, scrape toes
  • seen in bilateral periventricular lesions (ie cerebral palsy)
  • tight hip adductors–>scissoring gait can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neuropathic gait (steppage gait, equine gait)

A

seen in pts with foot drop (weakness of foot dorsiflexion)–>attempt to lift leg high enough during walking so the foot doesn’t drag on the floor

  • Unilateral: peroneal nerve palsy, L5 radiculopathy
  • Bilateral: ALS, CMT, uncontrolled diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Myopathic gait (waddling gait)

A
  • hip girdle muscles keep pelvis level with walking
  • weakness on one side leads to drop in pelvis on contralateral side while walking (Trendelenburg sign)
  • Bilateral weakness: dropping of pelvis on both sides during walking leading to waddling
  • pts w/ myopathies like musc dystrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bradykinetic (Parkinsonian) gait

A
  • rigidity and bradykinesia
  • Posture stooped with head and neck forward with flexion at the knees
  • slow little steps
  • hard to initiate steps
  • festination (inclination to take accel steps)
  • Parkinson’s disease or parkinsonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Choreiform gait (hyperkinetic gait)

A
  • central basal ganglia disorders (huntington’s; other forms of chorea, athetosis, dystonia)
  • Irregular, jerky movements in all extremities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ataxic gait

A
  • cerebellar disease
  • clumsy, staggering movements with WIDE based gait
  • no heel toe walk or straight line
  • truncal disability–>think vermis
17
Q

Sensory gait

A
  • loss of proprioceptive input
  • pt slams foot hard on ground to sense it
  • exacerbation in dark
  • “stomping gait”
  • in disorders of dorsal columns (B12 deficiency or tabes dorsalis) or diseases impacting peripheral nerves (diabetes)
18
Q

Synucleinopathies histologic hallmarks

A
  1. Parkinson disease= Lewy bodies, lewy neurites
  2. multiple system atrophy=axonal and neuronal inclusions; glial cytoplasmic inclusions

Altered alpha-synuclein leading to aggregation

19
Q

Tau protein deposition diseases (tauopathies)

A

Neurodegen changes in association with intraneuronal and/or intraglial inclusions composed of abnormally aggregated protein tau.
Tau normally binds to/stabilizes microtubules
-FTD
And primarily dementing disorders:
-Pick’s disease
-Alzheimer’s disease
-frontal lobe degen of non-Alz type

And tauopathies assoc with extrapyramidal disorders of movment:

  • PSP
  • Cortical basal degeneration
20
Q

Prion disease

A

misfolded protein (PrP)

21
Q

Parkinson’s Disease

A
  • most are sporadic, onset 50-60s
  • genes involved: mut in alpha synuclein, also Tau
  • loss of pigmented neurons, starting in lower brainstem nuclei (dorsal motor n X, locus coeruleus)
  • progressively involving substantia nigra (dopamine)
  • residual clusters of pigment
  • Lewy bodies
  • alpha synuclein (in Lewy body and in neuron processes–Lewy neurites)
  • spherical eosionphilic neuronal cytoplasmic inclusions= “lewy bodies”
22
Q

Diffuse Lewy Body Disease

A

-more diffuse Lewy body distribution in brain
-can be assoc. w/ dementia
-dementia with lewy bodies= onset of dementia within 1 year of onset of parkinsonism
[PD w/ dementia (PDD)=onset of dementia >1 yr after Parkinsonism onset)
-Diffuse Lewy body disease often co-exists w/ AD related neruitic plaques and neurofib tangles

23
Q

Multiple System Atrophy

A

-Neurodegen dis w/ a spectrum of overlapping clinical expression including:
parkinsonism
progressive ataxia
dysautonomia (Shy-Drager syndrome)

-alpha-synuclein

-Degeneration involves mult central systems:
striatonigral (MSA-P when park predom)
(olivo)pontocerebellar (MSA-C when cerebellar predom)
intermediolateral columns (including MSA-P and MSA-C)

Pathologically, defined by glial (esp oligodendroglial) alpha synuclein inclusions (pontine nuc, putamen, STN, limbic crtices, SN, ION, reticular formation)

  • Striatonigral degen (Parkinsonism) results in putamenal atrophy
  • Loss of striatal neruons w/ gliosis and loss of neuropil
  • assoc loss of striato-pallidal and external capuslar white matter tracts

-(olivo)pontocerebellar atrophy characterized by loss of neurons from pontine nuclei–>atrophy of basal pons, loss of myelinated pontocerebellar fibers in MCP. Loss of
pontocerebellar fibers is associated with degeneration of Purkinje cells; possibly via
secondary (transsynaptic) degeneration (with associated gliosis). Also seen is loss of
neurons from inferior olivary nuclei, which may be secondary (retrograde) resulting in
their atrophy with loss of myelinated olivocerebellar (“climbing”) fibers (with associated
gliosis).

-Intermediolateral column degeneration (with associated gliosis) – appears to
underlie dysautonomia seen in a third form of MSA (Shy-Drager syndrome).
Argyrophilic glial cytoplasmic inclusions are Alpha-synuclein- immunoreactive - now
considered a histologic hallmark of MSA

24
Q

Alzheimer’s Disease

A

Location: temporoparietal (starts in hippocampus)
Macro: cerebral atrophy
Micro: Abeta plaques, tangles

25
Q

Huntington disease

A 
Location: basal ganglia
Macro: neostriatal atrophy
Micro: neuronal loss and astrocytosis
-adult onset *40s
-Aut dom
-choreiform movement disorder
-can assoc w/ frontal lobe atrophy
-mut gene on chrom 4 (CAG trinuc repeat in huntingtin prot)
-anticipation
-progressive atrophy of neostriatum, esp in anterior caudate and dorsal putamen; gross atrophy of head of caudate; loss of medium spiny neurons of neostriatum
-accomp by astroglial rxn
26
Q

FTD

A

location: frontotemporal
Macro: cerebral atrophy
Micro: tau, Pick bodies

27
Q

PSP

A
  • movement disorder 50s-70s
  • degen in nigrostriatal system; in paramedian brainstem and cerebellar roof nuclei; degenerating neruons contain globose, tau, neurofib tangles
  • akinesia and rigidity, supranuclear gaze palsy, dysarthria or dysphagia (variable), and possible FTD
  • tau (neurofib tangles) in neurons and tau in cortical and subcortical glia (3 of: pallidum, STN, SN, or pons)
  • can include frontotemporal cortical atrophy – neruon loss and gliosis (demented)
  • 4R tau
28
Q

Corticobasal degeneration

A
  • movement disorder
  • 50-60s
  • clumsy, stiff, later rigid and akinetic, alien limb phenom
  • frontotemp dementia can occur too
  • cererbral cortical atrophy (peri-rolandic)
  • Tau inclusion in neruons in substantia nigra, locus ceruleus, tegmental and raphe nuclei, glia; striatum
  • “coiled bodies in oligodendroglia; “astrocytic plaques”
  • 4R tau
29
Q

Degenerative ataxias

A

Hereditary degen ataxias:

  • spinocerebellar ataxias
  • Freidreich ataxia

Also nonhereditary

  • “Primary” cerebellar cortical degen accomp by degen olivocerebellar pathways and often by spinocerebellar tract degen.
  • Olivopontocerebellar atrophy can be seen as degen pattern

They tend to present with atrophy of cerebellar folia, involving both cortex
and “digitate” white matter, associated with loss of Purkinje cells (“empty
baskets” and “torpedoes”) and Bergmann gliosis

30
Q

Friedreich’s ataxia

A

-rare, hereditary
-b/f 20y old
-AR*****
-chrom 9q, GAA triplet repeat expansion, frataxin prot–>mitochondrial dysfunc
limb ataxia, dysarthria, loss of distal position and vibration sense, upper
limb wasting, areflexia, can have upper motor neuron-like lower extremity weakness
-loss of neurons in DRG, loss of peripheral sensory fibers, and DC fibers, loss of cerebellar afferents, cerebellar efferents from dentate nuc, degen in corticospinal tracts
-loss of neurons in Clark’s column
-anterior horn cells spared

Neuro 3 (mine) (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions