Block VIII, Week I
Terms
undefined, object
copy deck
- the cytoplasmic granularity found in neurons is called?
- Nissl substance
- what type of stains are used for the best visualizations of neurons?
-
silver-based stains
("Beil" stain, Bodian stain) - T/F: neurons have no regenerative capacity
- True
- under what conditions would a neuron undergo chromatolysis?
-
when the axon is severed
(chromatolysis = swelling of cell body) - a neurological rabies infection would have what microscopic neuronal manifestation?
- inclusion bodies
- describe the microscopic characteristics of ischemic change in a neuron
-
pyknotic nucleus
red cytoplasm
"red-dead neurons" - what occurs in chromatolysis and what are the microscopic characteristics of it?
-
chromatolysis - severing of axon
see an eccentric nucleus, ground glass cytoplasm - function of astrocytes?
- transport substances from blood to CNS
- useful stains that help us visualize astrocytes? (3)
-
PTAH
GFAP
immunostain - MC reaction of astrocytes to injury?
- proliferation, cause gliosis (glial scar)
- what is the "gemistocytic change" sometimes seen in neuronal injury?
- astrocytes that are plump, round and have an abundant eosinophilic cytoplasm
- when are Alzheimer's type II astrocytes seen and what do they look like?
-
seen in hepatic failure
swollen, bizarre nuclei - when are Rosenthal fibers seen?
- in chronic gliosis
- stain used to best see myelin?
- luxol-fast blue
- reaction of oligodendrocytes to injury?
- most likely cell death with resulting myelin loss
- where are ependymal cells found?
- line the ventricular cavities and the neural tube
- function of choroid plexus?
- produces CSF by ultrafiltration
- changes seen in the ependymal lining when there is underlying astrocytic proliferation going on?
- ependymal granulations
- describe the ependymal cell
- ciliated cuboidal epithelial cell
- function of microglial cells?
- specialized CNS macrophages
- what is the stimulus for transformation of microglial cells to "rod cells?"
- injury causes proliferation of microglial cells with elongation of nuclei = rod cells
- what reaction does a microglial cell have to a virally infected neuron?
- attacks it
- how does a microglial cell become a foamy macrophage?
- it scavenges lipid in infarcted and demyelinated areas
- what stain is used to best visualize lipid-laden microglial cells?
-
oil-red-O stain
(orange is the lipid scavenged by the macrophages) - what are the four horizontal levels of a neuropathological lesion?
-
1. supratentorial
2. posterior fossa
3. spinal
4. peripheral - what are the 4 basic differentiations we should make in the clinic to evaluate a neurological problem?
-
1. anatomic level of lesion
2. focal or diffuse
3. progressive or nonprogressive
4. acute, subacute, chronic - most acute neuropathological incidents are of what etiology?
- vascular
- give an example of a focal, acute neuropathological incident
-
infarct
intraparenchymal hemorrhage - most subacute neuropathological incidents are of what etiology?
- inflammatory
- give an example of an acute, diffuse, neuropathological incident
-
subarachnoid hemorrhage
anoxia - give an example of a focal, subacute neuropathological etiology
- abscess
- give an example of a diffuse, subacute neuropathological etiology
- meningitis or encephalitis
- what is the most likely etiology of chronic, focal neuropathological symptoms?
- neoplasm
- what is the most likely etiology of chronic, diffuse neuropathological symptoms?
- degenerative
- what are the proposed mechanisms behind demyelinating disease? (3)
-
1. inflammatory (immune, autoimmune)
2. genetic
3. unknown - what type of demyelinating disease is characterized by a relapsing and remitting course?
- MS
- is MS characterized by focal or diffuse deficits?
-
focal
(distinct demyelinating lesions in the CNS) - when is the typical onset of MS?
- 3rd-4th decade
- F:M of MS?
- F:M = 2:1
- what pathways are impaired in MS?
-
visual
sensory
motor
coordination - two types of MS?
-
1. classic (Charcot) form
- most common, classic relapsing and remitting course with gradual overall decline
2. acute (Marburg) form
- young adults, rapidly progressive and unrelenting course - MS is most apparent in what portion of the brain and spinal cord?
-
white matter
(in MS you see gray matter plaques in white matter areas) - what is a shadow plaque?
- an older MS plaque that shows limited remyelination
- microscopic characteristics of the axons in MS?
- axons are relatively spared so they are most likely "normal" looking
- where in the brain is it common for MS plaques to appear?
- around the ventricles (esp. the lateral horns of the lateral ventricles)
- describe the borders of an MS plaque
- well circumscribed borders
- describe the immune pathogenesis of MS that Dr. Weiland gave.
-
* oligodendrocyte injury mediated by cytotoxic CD4+ T-cells
* see oligoclonal immunoglobulins in the CSF
* lymphocytic infiltrates in the plaques -
is there a genetic link for MS?
which HLA is MS associated with? -
* increased risk in 1st degree relatives, increased in twins
* associated w/HLA-DR2 - geographically, where is MS more common?
-
temperate zones
(risk conferred by 18 yrs of age) - which demyelinating disease is characterized by prominent visual and spinal cord involvement and NO cerebral or cerebellar involvement?
- neuromyelitis optica (Devic's disease)
- how can acute disseminated encephalomyelitis (ADEM) be distinguished from MS?
- ADEM is a diffuse demyelinating autoimmune disease, MS is a focal demyelinating autoimmune disease
- common etiologies of ADEM?
-
* often occurs after childhood viral illness (measles, rubella, VZV)
* vaccinations (rabies, mumps, rubella) - microscopic characteristics of ADEM?
- perivascular inflammatory infiltrates with demyelination (seen in entire brain)
- prognosis of ADEM?
- variable, but most mild cases completely recover
- describe acute hemorrhagic leukoencephalitis (AHL)
-
"hemorrhage with demyelination"
(a hyperacute form of ADEM with hemorrhage - often fatal within days) - micro characteristics of acute hemorrhagic leukoencephalitis? (4)
-
* perivascular demyelination
* inflammatory infiltrates
* fibrinoid necrosis
* punctate hemorrhages - symmetric non-inflammatory demyelination of the pons is known as?
- central pontine myelinolysis
- possible etiology of central pontine myelinolysis?
- * hyperosmolality due to rapid overcorrection of hyponatremia
- clinical features of central pontine myelinolysis?
- ranges from asymptomatic to flaccid quadraplegia to stupor or coma.
- leukodystrophies are hereditary disorders of?
- myelin production or metabolism
- metachromatic leukodystrophy is a defect in what enzyme? result?
-
defect in arylsulfatase A
*results in accumulation of sulfatides in oligodendrocytes - Krabbe disease is a defiency in?
- beta-galactosidase
- Adrenoleukodystrophy results in?
- high levels of very long chain fatty acids
- inheritance pattern of leukodystrophies?
- AR
- inheritance pattern of neuronal storage diseases?
- AR
- Tay-Sachs is a deficiency in?
-
hexosaminidase A
*result is accumulation of gangliosides - Hurler syndrome is a deficiency in?
-
a-iduronidase
* result is accumulation of mucopolysaccharides - Gaucher's disease is a deficiency in?
- glucocerebrosidase
- Neimann-Pick syndrome is a deficiency in?
- sphingomyelinase
- PKU is a deficiency in?
- phenylalanine hydroxylase (get accumulation of phenylalanine=neurotoxin)
- result of excess phenylalanine?
- irreversible mental retardation, seizures
- describe cretinism
-
congenital hypothyroidism
*see growth retardation, severe MR, deaf, mutism, motor spasticity/rigidity - neurological symptoms of Wilson's disease?
- dystonia, tremor, ataxia
- what is the location of CNS injury in wilson's disease?
- basal ganglia (esp. putamen, caudate nucleus)
- define spina bifida occulta
- vertebral arch defect
- describe a meningocele
- cyst like protrusion of the meninges
- describe a meningomyelocele
- cyst like protrusion of the meninges with nerve roots and spinal cord elements. (neurological problems are common)
- describe a rachischisis
- complete failure of closure of the caudal end of the neuropore
- describe anencephaly
- failed closure of the anterior neuropore
- describe Wernicke's encephalopathy
- acute deficiency of thiamine (B1) - manifests as confusion, opthalmoplegia, altered temperature regulation. FATAL if untreated.
- describe Korsakoff's syndrome
- chronic deficiency of B1 (thiamine) - see antegrade amnesia, confabulation
- in which thiamine deficiency are petechial lesions seen in the mammillary bodies?
- Wernicke's
- cardiovascular manifestations of a thiamine deficiency?
- Beriberi heart disease
- neurological manifestations of a B12 deficiency?
-
ataxia
(atrophy of posterior columns - position sense)
*sensory > motor deficits, dysesthesias common - which portion of the cerebellum is commonly atrophied in chronic alcoholism?
- cerebellar vermis
- besides atrophy of the cerebellar vermis, what other CNS changes are seen in relation to chronic alcoholism?
-
1. cortical atrophy
2. hydrocephalus-ex-vacuo (ventricles look larger due to cortical atrophy) - Parkinson's disease generally impairs voluntary or involuntary functions?
- involuntary functions
- what type of tremor is seen in PD?
-
resting
(may be absent in 1/4th of all PD patients) - avg. age of onset of PD?
- 45-60
- PD involves a loss of?
- DA neurons in the substantia nigra and locus ceruleus
- what are Lewy bodies composed of?
- a-synuclein
- what characterizes parkinsonism-dementia complex of Guam?
- parkinsonism w/ progressive dementia, death in 5-10 yrs
- how does progressive supranuclear palsy (PSP) differ from PD?
- PSP - no Lewy bodies, neuronal loss is in brainstem, basal ganglia, cerebellum
- some possible etiologies of parkinsonism? (4)
-
1. post encephalitic
2. drug induced
3. toxin related (MPTP)
4. repeated head trauma - inheritance pattern of HD?
- AD
- describe the progression of HD
-
early cognitive and emotional impairment
* then, extrapyramidal symptoms (choreoathetosis)
*eventual incapacitation - gross pathology of a brain with HD?
-
atrophy of frontal cortex, striatum
* secondary lateral ventricle enlargement - HD involves a mutation in a gene on which chromosome?
- chromosome 4
- MC genetic mutation type seen in HD?
- trinucleotide repeat expansion
- ALS involves which neurons?
- upper and lower MOTOR neurons
- describe the clinical course of ALS
-
* progressive muscular weakness
* atrophy, cramps, fasciculations
* motor speech disturbance
* intellect intact
* death usually w/i 3-5 yrs - avg. age of onset of ALS?
- 40-60 yrs
- gender differences in ALS?
- M>F
- familial ALS (5-10%) is related to a mutation in?
- superoxide dismutase 1 gene (SOD1)
- nervous system areas that atrophy in ALS?
-
* cortical motor neurons
* motor nuclei of brain stem
* loss of axons in LCST
* anterior horn spinal cord neurons
* anterior spinal nerve roots - which degenerative disease accounts for >50% of dementia
- AD
- characteristics of AD?
- progressive dementia with memory and cognitive impairment
- risk factors for AD? (3)
-
1. age
2. family history
3. female gender - what genetic disorder does AD have a strong connection to?
- Down's syndrome (trisomy 21)
- Four etiological factors that may contribute to AD?
-
1. amyloid beta
2. amyloid precursor protein
3. Apoprotein E e4
4. Presenilins - function of presenilins?
- create amyloid protein from amyloid precursor protein (APP)
- mutations in presenilins result in?
- most cases of familial AD
- which type of apolipoprotein has the lowest risk of AD?
- ApoE e2 or 3
- gross characteristics of AD?
-
*cortical atrophy (esp. frontal-parietal, temporal)
*atrophy of gyri, widening of sulci
* hydrocephalus ex vacuo - microscopic features of AD?
-
*neurofibrillary tangles
*neuritic plaques
*granulovascular degeneraton
*Hirano bodies - in AD, neurofibrillary tangles are primarily made up of what protein?
- tau (microtubule associated protein)
- in AD, what is found at the core of neuritic plaques?
- amyloid
- in AD, where is granulovascular degeneration found?
- in the cytoplasm of hippocampal neurons
- in AD, what are Hirano bodies?
- eosinophilic bodies by hippocampal neurons (seen alongside granulovascular degeneration)
- describe diffuse Lewy body disease
- dementia with Lewy bodies, may have accompanying akinetic rigidity syndrome (Parkinson like)
- gross characteristics of Lewy body dementia?
- not much, relatively little atrophy
- gross features of Pick's disease?
-
*marked cerebral atrophy limited to frontal and temporal lobes
*knife-blade gyri - what is a Pick body?
-
neurons with eosinophilic cytoplasmic inclusions - which stain is used to see Pick bodies?
- silver stain
- 50% of dementia can be classified as?
- AD
- dementia in which a personality change or language disorder is seen is called?
-
frontotemporal dementia
(10% of all dementias) - what must be present in order to make the diagnosis of dementia?
- acquired memory impairment WITH impairment in other domains (cognitive or social).
- how common is dementia?
-
5-10% of community dwelling adults over the age of 65
50% of those over the age of 80.
70% of all nursing home pts. - how can a person have cognitive impairment but not meet the definition of dementia?
- poor memory performance but NORMAL general cognition and ADLs
- what are some "reversible" causes of dementia? (7)
-
1. depression
2. medication
3. alcohol use
4. delerium
5. chronic menigitis
6. tumor
7. normal pressure hydrocephalus - describe progressive pseudodementia
-
paitents describe cognitive complaints, have difficulty encoding memories.
DURATION OF DEMENTIA IS SHORTER, depression common, antidepressant trial often warranted - List 5 medications commonly responsible for cognitive decline
-
1. pain meds
2. anticholinergics (amitryptiline, nortryptaline)
3. antihypertensives
4. psychotropics
5. sedative-hypnotics (sleeping pills) - how common is true inherited AD?
- <5%
- mean survival of an AD patient?
- 8.1 years
- MC cause of death in an AD patient?
- pneumonia
- physical manifestations of late AD?
-
increased tone,
myoclonus,
seizures,
bradykinesia,
incontinence,
dysphagia,
weight loss - psychiatric manifestations of AD?
-
depression
delusions
hallucinations
personality change - in which type of dementia are hallucinations very common?
- Lewy body dementia
- 6 risk factors for AD?
-
1. Apo-E4-Allele
2. Family history
3. age
4. female
5. head injury
6. lower intelligence/smaller head size - two pharmacologic treatments of AD?
-
1. acetylcholinesterase inhibitors
2. NMDA antagonists (Namenda) - what is the second leading cause of dementia?
-
Vascular dementia
(single stroke, multi-infarct, subcortical arteriosclerotic encephalopathy) - what is it called when vascular dementia is mixed with Alzheimer's pathology?
- mixed dementia
- describe the classic onset of vascular dementia
- sudden onset or stepwise deterioration
- how can vascular dementia be diagnosed?
-
abnormal imaging studies
(also see focal neurological signs and stroke risk factors) - what types of strokes cause dementia?
-
lacunar strokes
strategically placed "normal" stroke - what does a white matter change indicate?
- many things, SOMETIMES can indicate dementia and/or AD.
- what is the 3rd cause of dementia?
- subcortical arteriosclerotic encephalopathy (SAE), aka. Binswanger's disease
- where is demyelination and gliosis seen in subcortical arteriosclerotic encephalopathy?
- periventricular
- 3 psychological findings in SAE?
-
psychomotor retardation
apathy
abula (lack of initiative) - 5 physical findings in SAE?
-
1. pseudobulbar brainstem signs (trouble swallowing)
2. hypperreflexia
3. upgoing toes
4. gait disturbance
5. incontinence - treatment for multi-stroke dementia? (4)
-
*antithrombotic
*cholinesterase inhibitors
*memantine
*supportive, risk factor management - avg. age of onset of frontotemporal dementias?
- EARLY <65
- three distinct pathologies of frontotemporal dementia?
-
1. Pick's disease
2. Frontal lobe degeneration
3. progressive subcortical gliosis - what is semantic dementia?
-
fluent empty speech "verbal diarrhea"
(loss of knowledge about items, trouble with naming, word comprehension. grammar and pronunciation remains intact) - what is progressive nonfluent aphasia?
- nonfluent speech, progresses to muteness
- describe the progression of CJD
-
subacute dementia with myoclonus, rapidly progressive
*80% dead in 1 yr, 50% dead w/i 5 mo. - avg age of onset of CJD?
- 50-75 yrs
- pathogenesis of CJD?
- prion protein (PRP - normally an a-helix) changes conformation to a beta-pleated sheet (bad form: protease resistant). this form accumulates in neuronal tissue, causes neuronal death.
- 7 classical signs/symptoms of Parkinsonism?
-
1. rigidity
2. bradykinesia
3. tremor
4. stooped posture
5. instability
6. changes in handwriting
7. sleep disorders - T/F: DBS helps parkinsonism
-
FALSE
DBS only helps PD, not all cases of Parkinsonism - PD makes up for what proportion of parkinsonism cases?
- 2/3
- 5 other causes of parkinsonism?
-
1. PSP (progressive supranuclear palsy)
2. MSA (Multi-system atrophy)
3. CBD (Corticobasal degeneration)
4. LBD (Lewy body disease)
5. stroke
others - which two races have the lowest incidence of PD?
-
Asians
African Americans - voice changes seen in PD?
-
hypophonia
(soft, tremulous voice) - what clues suggest a diagnosis OTHER than PD? (7)
-
1. lack of tremor
2. prominent/early dementia
3. autonomic dysfunction
4. early instability/falls
5. eye movement difficulties
6. lack of response to levodopa
7. early hallucinations - how many DA neurons must be lost before motor symptoms appear in PD and a diagnosis is made?
- 80%
- how long before the onset of PD does loss of the DA neurons begin?
- 20-30 yrs prior
- early symptoms of PD? (5)
-
1. anxiety, depression
2. changes in sense of smell
3. constipation
4. postural changes
5. sleep disorder/weight loss - in the on-off phenomenon, what does the off phase correspond to?
- no DA stimulation
- in a PD patient, what are the leading cognitive risk factors for nursing home placement?
- delerium and dementia
- three stages of PD?
-
1. honeymoon period
2. battle area
3. late phase - which type of PD is thought to have a better prognosis?
- tremor predominant PD
- which 2 types of PD are thought to have a prolonged course?
-
unilateral disease
young patients - gold standard treatment of PD?
- Sinemet (carbidopa/levodopa)
- MOA of carbidopa/levadopa?
-
*levadopa causes peripheral side effects (toxic)
*carbidopa counteracts these peripheral side effects (MAO inhibitor, blocks levodopa breakdown into toxins in periophery) - how can nausea be treated in the PD patient on carbidopa/levadopa?
-
increase carbidopa
take with meals - 3 dopamine agonists used to treat PD?
-
1. Mirapex
2. Permax
3. Bromocriptine - neuroprotectant used to prevent progression of PD?
- Selegeline
- role of Entacapone (Comptan) in PD treatment?
- extends 1/2 life of levadopa
- 3 anticholinergics used to treat PD?
-
1. Congentin
2. Artane
3. Benadryl - MOA of Amantadine?
- NMDA antagonist
- in DBS for PD, where are the electrodes placed (1 of 3 locations)
-
1. globus pallidus
2. subthalamic nucleus
3. thalamus - 2 positive outcomes of surgery for PD?
-
1. improves time spent in "on" state
2. decreases need for meds - risks/negative outcomes of surgery for PD?
-
*risk of bleed, stroke, infx
*risk of masking dementia, dysarthria
*poor placement or equipment failure - characteristics of Lewy Body Dementia (DLBD) when it comes to meds?
- very sensitive to meds & their adverse effects - treat gingerly
- in which sex is DLBD more common?
- males
- MC of death in DLBD?
- aspiration pneumonia
- how long from symptoms to death in DLBD?
- 6.4 yrs
- where are the Lewy Bodies found in DLBD?
- dopaminergic neurons (diffusely located)
- treatment of DLBD?
-
1. low dose carbidopa/levadopa
2. low dose antipsychotic for hallucinations (quetiapine or clozapine)
3. AChE inhibitor for cognition, behavior problems
4. Klonopin for periodic limb movements of sleep - hallmark symptom of progressive supranuclear palsy (PSP)?
- supranuclear opthalmoplegia
- does PSP respond to levadopa?
- NO
- avg age of onset of PSP?
- 60s-70s
- regarding PSP: on average, how long after diagnosis does death occur?
- 6 yrs
- Treatment for PSP? (3)
-
1. Sinemet - limited motor response
2. SSRIs (depression/anxiety, pseudobulbar effect)
3. AChEIs for dementia - 3 variants of multiple system atrophy (MSA)?
-
1. Shy Drager syndrome (MSA-A)
2. striatonigral degeneration (MSA-B)
3. OPCA (MSA-C) - characteristics of MSA-A (Shy-Drager syndrome)?
- dysautonomia (faining, cold hands, mottling, incontinence)
- characteristics of striatonigral degeneration (MSA-B)?
- Parkinsonian symptoms
- characteristics of OPCA (MSA-C)
- ataxia
- treatment for MSA?
-
PT/Speech Therapy
early response to levadopa
fludrocortisone or midodrine for BP support - four causes of acquired ataxias?
-
1. alcohol
2. chemotherapy
3. infections
4. paraneoplastic - two inherited ataxias?
-
1. Friedreich's ataxia (AR)
2. Spinocerebellar ataxia (AD and sporatic) - what is the rarest Parkinsonian condition?
- Corticobasal degeneration
- age of onset of corticobasal degeneration?
- 60's or later
- s/s of corticobasal degeneration?
-
"alien limb phenomenon"
asymmetric parkinsonism and limb dystonia WITH UMN signs and late dementia - "lower-half" parkinsonism with prominent gait disturbance, subcortical dementia, AND a history of stroke is called?
- vascular parkinsonism
- what is the cause of dementia pugulistica?
- repeated head trauma
- s/s of dementia pugilistica?
-
*attentional and memory deficits
*parkinsonism - is there any genetic group that is at higher risk of dementia pugilistica?
- ApoE4 carriers
- symptomatic, communicating, adult onset hydrocephalus is known as?
- normal pressure hydrocephalus
- what is the triad seen in normal pressure hydrocephalus?
-
1. subcortical dementia (subacute)
2. frontal "magnetic" gait disturbance
3. urinary incontinence - what is frequently seen in normal pressure hydrocephalus?
-
parkinsonism
(with bradykinesia, rigidity, limb tremors) - causes of normal pressure hydrocephalus? (3)
-
1. remote trauma, infection
2. subarachnoid hemorrhage
3. idiopathic - of the triad seen in normal pressure hydrocephalus, which symptom is earliest?
- gait disturbance (apraxic gait - "stuck to floor" feeling)
- MRI findings in NPH?
-
1. ventriculomegaly
2. thinning of corpus callosum
3. no CSF flow - shunting is what is normally done to treat normal pressure hydrocephalus. when is it less effective?
- if small vessel disease is present
- success rates/results of shunting in NPH?
-
1/3 have marked improvement
1/4 have mild improvement
1/4 have moderate complications
1/4 have shunt malfunction - describe an essential tremor
-
tremor that is most promiment with intention.
*often distal in the limb - which type of tremor, resting or essential, is responsive to alcohol?
- essential
-
what am I?
hyperkinetic movements with irregular, unpredictable, brief, jerky movements that move from one part of the body to another... - chorea
- what is the difference between chorea and choreoathetosis?
- choreoathetosis is slower than the characteristically brisk chorea
-
what am I?
inherited, progressive disorder manifested by chorea and other movements, behavior disorder and dementia - HD
- inheritence pattern of HD?
- AD
- when do s/s of HD appear?
- in the 4th or 5th decade
- where is the HD gene and what happens genetically in HD?
-
chromosome 4
HD is the result of an expanded CAG trinucleotide sequence - genetic correlation between severity of the disease?
- increased number of repeats = increased severity of disease
- under which type of inheritance is the number of repeats in HD more likely to increase?
- father to child
- what type of reflexes would most likely be present in a HD patient?
-
brisk reflexes
upgoing toes - what part of the brain atrophies in HD?
- caudate
- what is the life expectancy after an HD diagnosis?
- 10-20 yrs
- MCC of death in HD?
- aspiration
- signifance of earlier onset HD as compared with "normal" onset?
- earlier onset has faster progression and seizures are more likely
- the condition of chronic dopamine receptor blockade is known as?
- tardive dyskinesia
- MC location of tardive dyskinesia?
-
around the face
(can occur in the body as well) -
what disorder am I?
disorder of sustained muscle contraction which creates abnormal posture? - dystonia
- generalized dystonia is often inherited. it is due to a mutation of?
- the DYT1 gene
- any treatment for dystonia?
-
dopamine
SOME are dopamine responsive, others are not - which type of dystonia often starts late in adult life?
- focal or segmental
- which sex is tics more common in?
- males
- age of onset of tics?
- childhood
- what is Tourette's syndrome?
- childhood onset of motor and vocal tics
- inheritance pattern of Tourette's syndrome (TS)?
- AD
- TS is commonly seen with what other conduct disorders? (2)
-
ADHD
OCD -
which disorder am I?
sudden, brief, shock-like involuntary movements - myoclonus
- myoclonus is seen in what brain diseases/injuries? (3)
-
1. hypoxic brain injury
2. late stage neurodegenerative diseases
3. early stage CJD - name three metabolic movement disorders with associated dementia
-
1. Wilsons disease
2. Hallevorden-Spatz
2. Idiopathic basal ganglia calcification - what is Hallevorden-Spatz disease?
- early onset dementia with parkinsonism - iron deposition in basal ganglia
- idiopathic basal ganglia calcification presents as?
-
dementia with parkinsonism
(familial disorder) - inheritance pattern of Wilsons disease?
- AR