Neuropsychological Disorders Flashcards
two-hit hypothesis/diathesis stress model/neurodevelopmental model of schizophrenia
developmental vulnerability that then emerges at specific ages of onset in response to stress
diagnostic tests for Alzheimer’s
Mini-mental state examination, Montreal Cognitive Assessment (MOCA) - screening measure, does not assess specific function
primary progressive aphasia
lose words
semantic dementia
lose understanding of word meaning
progressive non-fluent aphasia
lose Broca’s area, stops speaking
stroke
the sudden disruption of blood flow to the brain
infarct
area of dead or dying tissue resulting from an obstruction of the blood vessels
ischemia
disorders due to blockage in blood vessels going to the brain
thrombosis
formation of a plug or clot in the blood vessel
embolism
a clot or plug that is brought through the blood from a larger vessel to a smaller vessel
cerebral arteriosclerosis
thickening and hardening of the arteries
cerebral vascular insufficiency or transient ischemia
temporary ischemia, disorder has variable nature over passage of time
migraine stroke
accounts for a significant number of strokes in younger people, especially women, appears as a transient ischemic attack
symptoms of migraine stroke
impaired sensory function, numbness of the skin, difficulties moving, aphasia
cerebral hemorrhage
massive bleeding into the brain, most often caused by hypertension/high blood pressure
angioma
congenital collection of abnormal blood vessels that divert normal flow of blood, eg. arteriovenous malformation (AVM)
aneurysms
vascular dilation, due mostly to congenital defects/hypertension/arteriosclerosis/embolisms/infections
how do you treat cerebral vascular disorders?
- drug therapy (t-Pa therapy, neuroprotective drugs, antiplatelet agents)
- surgery (relieve pressure, metabolic syndromes increases surgical risk)
- prevention!
traumatic brain injuries - open-head injuries
TBIs with skull penetration, neurological signs/symptoms are highly specific, may undergo rapid and spontaneous recovery if injury is small and specific
traumatic brain injuries - closed-head injuries
coup, countercoup, twisting and shearing of major fiber tracts, bleeding and pressure can result in hematomas, edema: can produce coma, behavioural effects
coup
damage at the site of the blow
countercoup
damage at the opposite side of the blow due to pushing or pressure
coma
loss of consciousness; commonly accompanies closed-head injuries
behavioural effects of TBI
impairment of specific functions mediated by the cortex at site of damage, more generalized impairments from widespread trauma throughout brain
brain injuries subsequent to closed head trauma: primary brain injuries, immediate on impact
- coup and contrecoup contusions
- fiber shearing or stretching
- macroscopic and microscopic lesions
- laceration or depression from skull penetration or fracture
brain injuries subsequent to closed head trauma: secondary injuries
- intracranial hemorrhage and edema
- ischemic or bleed-induced damage
- increased intracranial pressure or distortion
- effects of multiple injuries and hypoxia
brain injuries subsequent to closed head trauma: injurious effects, delayed
degeneration of gray and white matter, hydrocephalus
what are behavioural assessments for head injury?
- Glasgow Coma Scale
- Posttraumatic Amnesia (PTA)
glasgow coma scale
objective indicator of the degree of unconsciousness and of recovery from it: measures eye opening, motor response, verbal response
posttraumatic amnesia
measure of severity of injury, correlates with future memory disturbance, no consistent method used for measurement of amnesia
epilepsy
brain disorder caused by recurrent seizures
symptomatic seizures
seizures identified with a specific cause
idiopathic seizures
appear spontaneously, without an apparent cause
what are 3 common symptoms of epilepsy?
1) onset of aura - warning of an impending seizures
2) loss of consciousness
3) motor component
what are 4 types of seizures
1) focal seizures
2) generalized seizures
3) akinetic seizures
4) myoclonic spasms
focal seizures
beings in one place (a focus point) and spreads
Jacksonian focal seizures
begins with movement in one part of the body and spreads
complex partial seizures
subjective experiences precede the attack, automatisms-automatic behaviours, postural changes
generalized seizures
bilaterally symmetrical,
grand mal attack
(generalized seizure) tonic stage, clonic stage, postseizures: postictal depression
petit mal attack
(generalized seizure) loss of awareness, no motor activity, brief duration
akinetic seizures
ordinarily only seen in children, child may collapse without any warning, attacks are short
myoclonic spasms
massive seizures, consists of sudden felxion or extension of the body
treatment of epilepsy
anticonvulsant drugs (diphenylhydantoin-DPH, dilantin; phenobarbital), surgery, DBS
tumours
mass of new tissue that persists and grows independently
benign tumour
not likely to recur after removal
malignant tumour
likely to recur after removal, progressive and life-threatening
encapsulated tumour
distinct entity, puts pressure on the brain (e.g. meningioma)
infiltrating tumour
not separated from surrounding tissue, may destroy healthy cells or interfere with cellular functioning (e.g. glioma)
glioma
arises from glial cells and infiltrates brain substance
meningioma
most benign of tumours, growths attached to the meninges, grows outside brain and well encapsulated
metastatic tumour
occurs in brain after tumour cells are transferred from elsewhere
treatments for brain tumours
- surgery
- radiation
- chemotherapy
classic migraine
- begins with aura that lasts for 20-40 mins (occurs as a result of vasoconstriction in the occipital cortex)
- headache
headache
occurs as vasodilation takes place, intense pain localized to one side, symptoms may include nausea and vomiting, can last hours-days
common migraine
most frequent type (80%), no clear aura, but another signal may presage attack
cluster headache
unilateral pain, short duration, but recurs repeatedly for weeks or months before disappearing
hemiplegic migraine and opthamologic migraine
relatively rare, loss of movement of limbs on one side and eyes respectively
treatments for migraine
- drugs
- ergotamine compounds (given with caffeine during acute attacks)
treatments for tension headaches
- muscle-relaxant drugs
- minor tranquilizers
- posture improvements
- reduction of stress
infection
invasion of the body by disease-producing microorganisms and subsequent tissue reactions
how do infections kill neural cells?
- interference with blood supply
- disturb glucose or oxygen metabolism
- alter cell membranes
- form pus
- causes edema
viral infections
caused by virus: encapsulated aggregate of nucleic acid made of either DNA or RNA
neurotropic viruses
e.g. rabies, polio: virus with special affinity for CNS cells
pantropic viruses
e.g. mumps, herpes: attacks other body tissues as well as CNS
bacterial infections
caused by bacteria; microorganism that has no chlorophyll and multiplies by simple division
bacterial meningitis
infection of the meninges by bacteria
brain abscesses
secondary to infection elsewhere in the body, cause cell necrosis and multiplication of bacteria increases intracranial pressure
mycotic infections
invasion of the nervous system by a fungus
parasitic infestations
- amebiasis (amebic dysentery: caused by infestation of a protozoan amoeba, results in encephalitis and brain abscesses)
- malaria (transmitted by bites of infected mosquitoes, produces local hemorrhages and subsequent degeneration of neurons)
treatments for CNS infections:
- viral infections (no specific antidotes except for rabies)
- bacterial cerebral infections (antibiotics, drain abscesses or do spinal tap to remove fluid)
- mycotic or parasitic infections (antibiotics used to treat associated disorders)
apraxia
inability, in the absence of paralysis or other motor or sensory impairments, to make or copy voluntary movements. usually follows damage to the neocortex
ataxia
failure of muscle coordination or irregularity of muscular action, commonly follows cerebellar damage
athetosis
ceaseless slow, sinuous, writhing movements, especially in the hands, due to abnormal function of the extrapyramidal system
catalepsy
muscular rigidity in which voluntary movements are reduced or absent but posture is maintained. a feature of PD due to da loss
cataplexy
complete loss of movement and posture during which muscle tone is absent but consciousness is spared
chorea
literally “to dance” ; refers to a wide variety of ceaseless, jerky movements that appear well-coordinated but are performed involuntarily
hemiplegia
complete or partial paralysis to one half of the body, usually follows damage to the contralateral motor cortex
palsy
usually refers to persisting movement disorders due to brain damage acquired perinatally
paralysis
complete loss of movement (more commonly) or sensation in a part of the body. usually permanent after damage to motor neurons, temporary after damage to motor cortex
paraplegia
paralysis or paresis of the lower torso and legs following spinal-cord damage
spasticity
increased tone in certain muscle groups that maintain posture against the force of gravity
tardive dyskinesia
slow, persistent movements, particularly of the mouth and tongue, usually follows long-term treatment with antipsychotic drugs
myasthenia gravis
severe muscular weakness; muscular fatigue after little effort; caused by insufficient acetylcholine receptors on muscles
treatment for myasthenia gravis
acetylcholine therapy to relieve symptoms, thymectomy and immunosuppressive drugs
poliomyelitis
infectious disease by a virus that has affinity for the spinal cord motor neurons and sometimes motor neurons of cranial nerves, causes paralysis and wasting of the muscles due to motor neurons loss
occurrence of poliomyelitis is controlled with:
Salk and Sabin vaccines
multiple sclerosis
due to loss of myelin, mainly in motor tracts
sclerotic plaques
small, hard, circumscribed scars where the myelin sheath has been destroyed
paraplegia
paralysis of the lower limbs caused by complete transection of the spinal cord
immediate symptoms of paraplegia
loss of movement, sensation, and reflexes, loss of thermoregulatory activity, loss of bladder control; some reflexes may gradually return
Brown-Sequard syndrome
unilateral section through the spinal cord
if loss is contralateral to the side of section:
loss of pain and temperature sensation, fine touch and pressure preserved
if loss is ipsilateral to the side of section:
preservation of pain and temperature, loss of fine touch and pressure, loss of sensation and voluntary movements distally
hemiplegia
loss of voluntary movement on one side of the body, changes in postural tone, and changes in various reflexes: damage is to neocortex and basal ganglia: changes in reflexes (appearance of the Babinski sign, loss of abdominal reflex and cremasteric reflex in males)
polygraph
records brain waves, on EEG
electromyogram
records muscle activity
electrooculogram
records eye movements
thermometer
records body temperature
narcolepsy
inappropriate and overwhelming attack of sleep, symptoms: sleep attacks, cataplexy, sleep paralysis, hypnagogic hallucinations
sleep attacks
brief, irresistible attacks of sleep; slow-wave NREM sleep, can occur at any time
cataplexy
complete loss of muscle tone, person can collapse or fall, probably an attack of REM sleep, occurs at times of emotional excitement
sleep paralysis
occurs in the transition between wakefulness and sleep, brief paralysis associated with the dream state but the person has woken up
hypnagogic hallucination
episodes of auditory, visual, or tactile hallucinations during sleep paralysis as person is waking up or going to sleep, can be frightening and intermixed with real events
insomnia
decreased REM, go through more transitions between stages, move more during sleep
sleep apnea
periodic cessation of respiration during sleep
obstructive sleep apnea
occurs in dream sleep and may be caused by a collapse of the oropharynx during dream sleep paralysis
central sleep apnea
CNS disorders, characterized by a failure of the diaphragm and accessory muscles to move, can be caused or aggravated by obesity
alzheimer’s disease
early impairment of declarative memory, some cognitive fluctuation, usually no motor symptoms, senile plaque density and neurofibrillary tangles
dementia with Lewy Body
early impairment in attention and visual-spatial skills, lots of cognitive fluctuation, visual hallucinations, motor symptoms (pronounced rigidity and bradykinesia); seen senile plaque density, some NFT, subcortical Lewy body, lots of cortical Lewy bodies
Parkinson disease
impaired executive functioning, some visual hallucinations late in disease course, motor symptoms are the initial manifestation of the disease and are generally unilateral, subcortical Lewy bodies present
FTD with main complaint being behaviour:
subtype of FTD = behavioural/dysexecutive (frontal variant FTD or R temporal variant FTD)
FTD with main complaint being language:
subtype of FTD = primary progressive aphasia (PPA)
fluent = semantic dementia SD, L temporal variant FTD) (non-fluent = progressive non-fluent aphasia (PNFA
memory deficits in Alzheimer’s disease:
episodic memory, semantic memory, working memory
memory deficits in frontotemporal dementia:
episodic memory, semantic memory, working memory
memory deficits in semantic dementia
some episodic memory, semantic memory
memory deficits in Lewy body dementia:
episodic memory and working memory
memory deficits in vascular dementia
some episodic/semantic/procedural memory, working memory
memory deficits in Parkinson’s diase
some episodic/semantic, procedural memory, working memory
schizophrenia symptoms:
1) delusions or beliefs that distort reality
2) hallucinations
3) disorganized speech, senseless rhyming
4) disorganized or excessively agitated behaviour
5) other symptoms that cause social or occupational dysfunction
biochemical abnormalities in schizophrenia
- dopaminergic function
- glutamate and glutamate receptors (decreased glutamate transmission)
- GABA and GABA binding sites
in schizophrenia, abnormal DA/GABA/Glu inputs to PFC:
impair DLPFC connectivity leading to DLPFC and cognitive dysfunction
clinical depression
(mood disorder): prolonged feelings of worthlessness and guilt, general slowing of behaviour, disruption of eating/sleeping
mania
(mood disorder): excessive euphoria, hyperactivity
bipolar disorder
(mood disorder): periods of depression and mania
abnormalities in depression
- decreased activity in DL and MPFC (reduced memory and attention)
- increased activity in orbital regions (attempt to inhibit amygdala activity and break persistent negative thoughts)
- increased activity of amygdala (increase HPA axis activity)
- increased activity of thalamus
sensitization model of bipolar disorder
large individual differences in degree of sensitization and drug effects in lab animals and
in Huntington’s disease
ACh and GABA neurons in the basal ganglia die, so there is no activation of inhibitory dopamine neurons in the substantia nigra
3 stages of Tourette’s syndrome
1) multiple tics
2) inarticulate cries
3) emission of articular words (echolalia, copralalia)
treatment of Tourette’s syndrome
antidopaminergic drugs, norepinephrine receptor agonists
major disease symptoms of Parkinson’s:
muscular rigidity, tremor, involuntary movements, postural disturbances
positive symptoms of Parkinson’s
tremor at rest, muscular rigidity (cogwheel rigidity - muscles move in series of steps), involuntary movements (akathesia, oculogyric crisis)
akathesia
cruel restlessness
oculogyric crisis
involuntary turns of the head and eyes to the side
negative symptoms of Parkinson’s
postural disorders (disorders of fixation and equilibrium), righting disorders, locomotive disorders (difficulty initiating stepping, festination-taking steps faster and faster), speech disturbances (lack of tone in voice), akinesia (slowness of movement)
WAIS
Weschler Adult Intelligence Scale = measures intelligence and cognitive ability
major neurodegenerative disorder (NCD)
substantial cognitive decline, sufficient to interfere with independent function, must not be attributable to another disorder
mild neurocognitive disorder (mild NCD)
modest cognitive decline, deficits don’t interfere with functioning independently
what are 5 types of dementias?
1) tauopathies
2) synucleinopathies
3) vascular dementias and vascular cognitive impairment
4) mixed dementias
5) other dementias
tauopathies
accumulation of tau proteins inside neurons
- alzheimer’s disease
- corticobasal degeneration (neuron loss and shrinkage in cortex and basal ganglia)
- frontotemporal disorders
- progressive supranuclear palsy (PSP): neuron loss in upper brainstem
synucleinopathies
accumulation of alpha-synuclein protein in neurons
- Lewy body dementia
- Parkinson’s disease dementia
vascular dementias and vascular cognitive impairment
injuries to cerebral blood vessels
- multi-infarct dementia
- subcortical vascular dementia (binswanger’s disease)
mixed dementias
combination of disorders such as Alzheimer’s and vascular symptoms
other dementias
- prion-related ementias (Creutzfeld-Jakob disease)
- Huntington’s disease
- secondary dementias
- head injury
- infectious dementias (AIDS dementia, syphilis)
- drug-related dementias (chronic alcohol)
which transmitter systems are changed in Alzheimer’s disease?
ACh, noradrenaline, DA, 5-HT and glutamate
