Neuro 3 Flashcards
Hypogeusia
reduced sense of taste
Ageusia
loss of taste (almost never)
Dysgeusia
is a condition in which a foul, salty, rancid, or metallic taste sensation persists in the mouth
can be complication of chemo- or radiation therapy
Xerostomia
(dry mouth) can also contribute to taste disorders
Hyposmia
reduced ability to detect odors.
Anosmia
complete inability to detect odors.
Parosmia
a change in the normal perception of odors, such as when the smell of something familiar is distorted, or when something that normally smells pleasant now smells foul.
Phantosmia
the sensation of an odor that isn’t there.
Impaired odor identification
can detect odor and know its different from other but can’t label
causes of olfactory disorders
Can occur following head trauma, chemical exposure (ZnSO4), smoking, nasal passage obstruction, central neuropathology
Olfactory changes with neurological disorders
dementia schizophrenia Parkinson's PTSD Depression Developmental insults
stimulation of amygdala leads to
fear
damage to amygdala results in
decreased conditioned fear response
Hebb’s rule
Long-term potentiation, a cellular model of synaptic plasticity, is a leading candidate mechanism underlying associative learning.
Necessity of thalamo-lateral amygdala synapses
shown necessary for acquisition and expression of conditioned fear.
Kluver-Bucy syndrome cause
Results from bilateral destruction of amygdala.
Characteristics of Kluver-Bucy syndromes
Hypersexuality (incl. inappropriate objects)
Hyperorality (examine objects by mouth)
Docility
Hyperphagia (incl. inappropriate objects)
Visual agnosia (cannot recognize familiar objects/people)
prefrontal cortex does what to amygdala
exerts inhibitory control over amygdala and emotion
limbic-motor interface
nucleus accumbens
interface between emotion and cognition
cingulate cortex
Anterior cingulate receives
reward-related signals from the ventral tegmental dopamine cell group and fear-related signals from amygdala.
Electrical stimulation of dorsal AC
anticipation of movement
Electrical stimulation of ventral AC
intense fear or pleasure
Anterior cingulotomy can relieve
chronic intractable pain,
treatment-resistant depression, OCD
bilateral removal of temporal lobes
anterograde amnesia
damage to hippocampus does not effect
perceptual learning (e.g., recognize faces, melodies) sensory-response learning (e.g., conditioned eye blink) motor learning (e.g., weaving)
damage extending into limbic cortex of medial temporal lobe
retrograde amnesia
Loss of ACh neurons in
Alzheimer’s disease
neuropathology of Alzheimer’s disease
Neuritic Plaques
Neurofibrillary Tangles
Congophilic Angiopathy
Synaptic Loss
2 hallmarks of alzheimer’s pathology
amyloid plaque
neurofibrillary tangles
tauopathies examples
alzheimer's disease fronto-temporal dimentia encephalopathy supranuclear palsy corticobasal degeneration Down's syndrome
alzheimers age of onset
familial: 65 yr
alzheimer’s genes
presenillin 1, 2
amyloid precursor protein (APP)
environmental causes of alzheimers
age head trauma high BO high cholesterol diabetes stroke
inherited factors of sporadic alzheimers
Apo E isoform
first degree relative
ApoE
colocalizes with A beta in plaques
strongest genetic risk factor for sporadic AD
homo- or heterozygous: 2-10X increased risk
small vessel disease
Ischemic white matter degeneration
Lacunar infarction of structures
Congophilic angiopathy
Binswanger’s disease
Arterioles show thickened walls, infiltration with lipid and widened peri-vascular spaces.
Perivascular demyelination resulting from vessel pathology
Lewy body dementia
Second most common form of degenerative dementia
Early psychotic symptoms: visual hallucinations, delusions
Parkinsonism
Fluctuations/diurnal variations in attention, arousal, or behavior
Orthostatic hypotension, syncope
Depression
Neuroleptic sensitivity
REM sleep behavior disorder
Probable LBD
Dementia
Two or more: marked fluctuations, visual hallucinations, parkinsonism
Presentation of fronto-temporal lobar degeneration
Gradual and progressive change in behavior
Gradual and progressive language dysfunction
Prion diseases
characterized by the conformational conversion of cellular prion protein (PrPc) into abnormal forms (PrPSc) that have high content of b-sheet structure and a strong tendency to aggregate and form amyloid fibrils
Jakob-Creutzfeld Disease
Most common prion disease;
Age at onset 60yr
Rapidly progressive with death
Clinical course of CJD
- swiftly progressing cognitive impairment
- behavioral alterations
- myoclonus
- ataxia
stroke definition
Sudden focal neurological symptom, attributed to a problem with blood vessels
two subtypes of stroke
Ischemic (lack of blood flow) > 80%
Hemorrhagic
TIA definition
Transient focal neurological deficit due to ischemia
Traditional Definition:
Less than 24 hours (usually
ACA symptoms
Contralateral LE weakness and sensory loss
Mental status impairment—confusion, amnesia, perseveration, personality changes, apathy
Abulia (inability to make decisions or perform voluntary acts)
MCA symptoms
Contralateral hemiparesis and/or hemisensory loss (Face + UE > LE)
Contralateral homonymous hemianopia
Dominant (usually L) hemisphere: Aphasia, alexia, agraphia, or acalculia
Non-dominant (R) hemisphere: Neglect, extinction, or spatial disorientation
VB symptoms (Vertebrobasilar)
“Crossed findings”
Contralateral hemi- or quadraparesis, dysarthria
Ipsilateral numbness and weakness of face
Cranial nerve palsies
Vertigo, nausea, ataxia, clumsiness
Diplopia, nystagmus, ophthalmoplegia
Diminished level of consciousness
PCA symptoms
Contralateral HH, cortical blindness, lack of depth perception, visual hallucinations
Perseveration and dyslexia
Contralateral sensory loss
Pupillary dysfunction, nystagmus, loss of conjugate gaze
Common clinical stroke symptoms
Weakness Impaired language (aphasia) Vision loss Numbness Gait disturbance Slurred speech
What’s missing from stroke symptoms
PAIN
thrombotic stroke mechanism
clot “in-residence”
embolic stroke mechanism
traveling clot
cardioembolic risk factors
Atrial fibrillation Recent anterior wall MI Left ventricular thrombus Left atrial thrombus Mechanical prosthetic valve Infectious endocarditis
Small vessel disease
Lacunar stroke
Small infarcts involving subcortical structures of the brain:
Internal capsule, basal ganglia, thalamus
Lacunar syndromes
Pure motor Pure sensory Sensorimotor Ataxic hemiparesis Clumsy hand-dysarthria Hemiballismus-hemichorea
aphasia
problem with language
inability to perform learned movements
apraxia
prosopagnosia
can’t recognize faces
R PCA/parietal
simultagnosia
can’t get visual gestalt
R MCA/diffuse
Broca’s aphasia
difficulty with expression
Wernicke’s aphasia
difficulty with receptive language
synesthesia
cross modal perception such as letter perceived as color
consciousness definition
state of full awareness of the self and one’s relationship to the environment
content, arousal
delirium definition
confusional state characterized by:
rapid onset
fluctuatic course
impairments of many systems
delirium produces alterations in
consciousness attention sleep-wake cycles cognitive abilities memory
delirium can manifest with
hypo or hyperactivity
hallucinations
delusions
delirium is NOT
dementia
causes/risk factors of delirium
primary brain disorders
systemic/general medical disorders
substances/withdrawal related
delirium treatment
treat underlying cause
behavioral control often necessary
early symptoms of DT
0-48 hours after last drink
tremulousness
hallucinosis
seizures
late symptoms of DT
48-72 hours after last drink fluctuating periods of confusion/clarity psychomotor agitation delusions frank hallucinations inattentiveness severe tremulousness dysautonomia (fatal)
treatment for DT
PRN diazepam is mainstay
alternative treatment for DT
ativan
medical complications of DT
dehydration, hypotension
Wernicke’s syndrome
global confusional state
opthalmoparesis
gait ataxia
appears over days to weeks, resulting from B1 deficiency
Korsakoff’s dementia
anterograde and retrograde amnesia
confabulation
impaired insight
alertness, attention, behavior preserved
Wernicke-Korsakoff damages which structures
maxillary bodies/hypothalamus
dorsomedial and anterior thalamic nuclei
coma definition
state of unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli
coma in practice
acute, temporary
no response to external stimuli
eyes are closed, do not open
sleep-wake cycles absent
3 areas of consciousness
reticular activating system
bilateral thalami
bilateral cortical dysfunction
if coma exam localizes to brainstem
likely structural lesion
if coma exam localizes to hemisphere
likely systemic illness
major elements of coma exam
Motor Response to External Stimuli
Pupils
Eye Movements
Breathing
normal oculovestibular reflex
the eyes deviate slowly toward the side of the cold water. The cortex corrects the deviation and the eyes then jerk back toward midline
coma oculovestibular reflex
absence of the slow deviation equals brainstem dysfunction. Absence of the corrective nystagmus implies cortical dysfunction.
when do adults emerge from coma?
2-4 weeks
persistent vegetative state- timing
1 month
brain death
no brain function detectable on neurological exam
all brainstem reflexes absent (including respirations)
major goal of coma exam
distinguish between diffuse cortical dysfunction and brainstem dysfunction
exclude mimics
diffuse cortical dysfunction
results from systemic abnormalities
brainstem dysfunction
structural injury
Gurstmen’s syndrome
finger agnosia (can’t name them)
trouble writing
trouble with math (acalculia)
Binswanger’s disease presentation
progressive cognitive decline with hemiparesis, hemianopsia and aphasia
