Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuro > 18: movement disorders > Flashcards

18: movement disorders Flashcards

1
Q

Hypokinetic movement disorders

A

parkinson’s
progressive supranuclear palsy
mutliple system atrophy

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

neurological features of PD

A

Asymmetric onset-later bilateral
Primary Extrapyramidal Features

Rigidity
resting tremor
bradykinesia
postural instability -late

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

PD- REM sleep behavior disorder

A

ndividuals retain the ability to move during dreaming and, thus, may “act out” their dreams with hitting, kicking, hollering, and even jumping out of bed.

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

gross pathological features of PD

A

degeneration of pigmented neurons

  1. substantia nigra pars compact
  2. locus ceruleus
  3. dorsal vagal nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

microscopic pathological features of PD

A

Lewy body formation

  1. CNS-pigmented
  2. ENS-non-pigmented
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

microscopic inclusions found in surviving pigmented neurons

A

lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

primary component of lewy bodies

A

synuclein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

primary NT deficit in PD

A

dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

parkinsonism plus syndrome

A

progressive supranuclear palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

clinical features of PSp

A

extrapyramidal features
rigidity-especially axial
neck hyperextension

bradykinesia
astoniched facies
dysarthria
life expectancy 10 years

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

neuro features of PSP

A

gait disturbances-early
postural; instability-falling
unexplained falling
tremor is unusual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

distinguishing feature of PSP that seprates it from PD

A

development of characteristic eye movement

supranuclear gaze palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

desribe supranuclear gaze palsy

A

impairment of volitional downgaze
(PD has difficulty with upgaze)

PSP then gets difficulty with upgaze and horizaontal gaze late

apraxia-unable to open closed eyes
-oculocephalic meneuver in tact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

gross anatomic pathologic features of PSP

A

midbrain ad cerebral cortical atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

microscopic PSP features

A

neuronal loss and gliosis of SN , and peduncolopontine of rostral midbrain, also GPE and GPI,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pathological hallmark of PSP

A

Neurofibrillary tangles, composed of unpaired straight filaments that contain abnormally phosphorylated tau protein are a pathological hallmark of PSP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tauopathy

A

PSP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

synucleinopathy

A

PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Most prominent nrueochemical abnormality fo PSP

A

Nigrostriatal Dopa deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

another Parkansonism plsu syndrome

A

Multiple System atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

three presentations of MSA (originally thought to be three diseases)

A

clinical picture of parkinsonism,

some with progressive autonomic failure

some with cerebellar syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

clinical features of MSA

A

RIGIDITY
BRADYKINESIA
POSTURAL INSTABILITY AND FALLING-EARLY
TREMOR UNUSUAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DOES MSA RESPONE TO LEVODOPA

A

SOME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CLINICAL HALLMARK OF MSA THAT SEPARATES IT

-78%

A

PROGRESSIVE AUTONOMIC FAILURE
-78%

URINARY DYSFUNCTION
ORTHOSTATIC HYPOTENSION
IMPOTENCE
GI DYSFUNCTION
THERMOREGULATORY DYSFUNCTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
MOST COMMON AUTONOMIC DYSFUNCTION SEEN IN MSA
ORTHOSTATIC HYPOTENSION
26
CEREBELLAR DYSFUNCTION ON MSA LESS COMMON | -55%
ATAXIA, DYSARTHRIA, OCULOMOTOR ABNORMALITIES, EXAGGERATED REBOUND
27
PYRAMIDAL SIGNS IN MSA-61%
HYPERREFLEXIA BABINSKI SPASTICITY PESUOBULBAR PALSY
28
DOES DEMENTIA DEVELOP WITH MSA
NOT TYPICALLY -SOME CONSIDER IT AN EXCLUSION CRITERIA FOR MSA BUT FRONTAL LOBE EXECTIVE FUNCTION DECLINES
29
OTHER UNIQUE FEATURES IN SOME MSA PATIENTS
Respiratory (laryngeal) stridor, probably produced in most instances by vocal cord abductor weakness, may develop in approximately one-third of patients with MSA and confers an increased risk of sudden nocturnal death. Involuntary sighing, Raynaud’s phenomenon, and postural myoclonus of the hand
30
MICROSCOPIC HALLMARK OF MSA
GLIAL CYTOPLASMIC INCLUSION BODIES THAT STAIN FOR ALPHA SYNUCLEIN
31
SYNUCLEINOPATHIES
PD AND MSA
32
MSA CHARATERIZED BY CELL LOFF AND GLIOSIS OF
BASAL GANGLA BRAINSTEM, CEREBELLUM SPINAL CORD CORTEX USUALLY UNAFFECTED**`
33
HYPERKINETIC MOVEMENT DISORDERS
HUNTINGTON'S TOURRETTE'S PRIMARY (IDIOPATHIC) DYSTONIA
34
INHERITANCE PATTER OF HD
``` autosomal dominant shorp arm of 4 -expanded trinucleotide CAG repeats -codes for huntingtin protein -too much causes neuronal cell damage ```
35
hallmark of HD
chorea-random, rapid jerky movements, that flow form one movement into tanother and impart a restless wiggly or dancingb appearance to the affected patient
36
neuro features of HD
``` chorea early dystonia with progression hyperkinetic dysarthria Parkinsonism in juvenile form Parkinsonism in advanced disease ```
37
other dominant clinical features of HD | *may be the initial disease symptom
behavioral changes ``` impulsiveness irritability obsessive behavior aggression depression dementia ```
38
eye dysfunction in HD
cant initiate saccades, slowed sccades, gaze impersistence
39
path features of HD especially in the caudate/putamen and cortex
Striatum--> caudate neuron and glial closs atrophy of GPallidus Cortex-< atrophy neuronal loss
40
defining feature of TS
tics | sudden sterotypes non-rhythmic movements or vocalizations
41
motor tics
simple or complex-preceded by premonition or urge that is satiated by making the movement
42
hallmark of TS progression
compliment of tics changes-some dissappear to be replaced by new ones *frequency and severity of tics waxes and wanes over time
43
formal Dx of tourrettes
multple motor and at least one vocal tic must be present at some point during the course, though not necessarily concurrenlty must occyre many times a day, almost every day, or intermittently over the course of more than abyear, with no more than 3 consecutive free months onset before 18 not explained by anything else
44
incoluntary gestures and words respectively
copropraxia coprolalia
45
other conditions seen in a high prevalence with TS
ADHD 90% and OCD 50%
46
dopa disturbance with TS?
TOO MUCH-responds somewhat to dopa inhibition
47
dystonia clinical picture
sustained muscle contraction producing sustained anc repetitive twisting movements resulting in abnormal psotures
48
inheritance pattern of dystonia
``` onset during childhood autosomal dominant DYT1 gene mutation on chromosome 9 glutamate deletion in torsin A penetrance is 40% worse in askinazi jews ```
49
pathological changes of dystonia
no consistent abnormality basal ganglia and cerebellum are proposed
50
neurchemical abnormality in dystonia
no constitent chemical found some suggest dopa., noradrenergic, GABAergic
51
focal dystonia arises in
adulthood and appears to have no genetic basis-unlike generalized dystonia
52
as dystonia (gen and focal) progresses it geenerally becomes
static
53
Mixed hypokinetic and hyperkinetic movement disease
wilsons dz
54
mutation in copper transporting ATPase
wilsons disease
55
inheritance pattern of wilsons dz
autosomal recessive long arm of 13 gene product is ATPB7-copper transporting ATPase
56
ATP7b utation
within liver,cannot transport Cu to apocerulopasmin forming ceruloplasmin - under conditions of elevated copper in the plasma-ATp7B causes biliary excretion of copper - copper accumulates in the liver
57
copper accumulation in the liver
wilson's disease
58
three areas affected by wilsons disease
1. hepatic is most common and in 12-15 yo 2. neurologic 3. psychiatric-19 year old
59
hypo/hyper neuro disorders of wilsons
``` parkinsonism chorea dystonia kindetic intention tremor (defining) dysrthria incoordination ```
60
opthalmologic features of Wilsons Disease
``` Kayser fleicher (descemet's_ rings suflower catarcts (lens accumulation) ```
61
in wilsons dz the copper in a KF ring accumulates in the
outer rim of cornea in Descemets membrane
62
neuro path features of wilsons
putamen, thalamus, cerebral cortex neuronal loss and gliosis OPALSKI CELL FORMATION *FROM DEGENERATING ASTROCYTES

Neuro (19 decks)

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