conditions Flashcards
what is Anencephaly? why is it important?
-Infection with the Zika virus in pregnant women can reportedly lead to insufficient development of parts/levels of the brain of a fetus.
( for ex: baby can have cerebellum but no cortex)
- it illustrateshe brain hirarchy
What is Huntington’s disease?
(hyperkinesia)
-Excessive movement(like touretts)
-Genetic mutation that results in the death of brain cells in basal ganglia(Damage to cells of the caudate nucleus)
and frontal lobes
-Neurodegenerative disease – progresses with age
-progressive dysfunction and death of cells of the Basal Ganglia -hyperkinetic syndrome; primary feature = excessive movement
- associated with a ‘hyperactive’ dopamine (DA) system (CH 5)
symptoms:
Motor symptoms:
Chorea (uncontrolled movements): + Symptoms
Slurred speech: - symptom
Loss of coordination: -symptom
Cognitive & emotional symptoms:
Memory and concentration problems:-
Impulsivity, disinhibition:+
Mood swings, depression, Irritability:-
Development of dementia:-
what does Parkinson’s disease consist of?
(hypokinesia )
- Basal ganglia( Damage to substantia nigra – dopamine nuclei)
-Loss of dopamine-producing cells in substantia nigra (“black matter”)
-can be familial or sporadic
-Pathology: loss of neurons, which often goes together with accumulation of “Lewy bodies” (protein clumps) in the brain
-less supply of dopamine (DA) to dopamine-dependent structures, like basal ganglia
symptoms:
motor symptoms:
-Loss of movement:-
congitive\emotional symptoms:
-depression, :-
-apathy,:-
- fatigue:-
-Problems in reward & punishment learning, cognitive flexibility
pathway:
Direct Pathway: With reduced dopamine, there is decreased activation of D1 receptors on MSNs in the striatum. This leads to less disinhibition of the thalamus and reduced facilitation of voluntary movements.
Indirect Pathway: With reduced dopamine, there is increased activation of D2 receptors on MSNs in the striatum. This leads to enhanced inhibition of the GPe, which in turn increases STN activity and ultimately increases inhibition of the GPi.
what are negative and positive symptoms?
-Positive symptoms: These are behaviours or experiences that are added to normal functioning. They often represent an excess or distortion of normal functions.
-Negative Symptoms: These involve a loss or decrease of normal functions.
what is cognitive slowing?
-one of the main effects of brain damage
-it’s the slowing down of cognitive processes ( most likely because of a loss of sensory representations so we end up relying on elementary representations)
what is Hemiparesis?
-weakness or partial paralysis that affects one side of the body
-usually due to damage in motor areas (M1)
what is Hemiplegia?
-paralysis or severe weakness that affects one entire side of the body
-damage to motor cortex (ex: M1)
what is Spasticity?
- stiffness and involuntary muscle spasms or contractions.
-occur following damage to the central nervous system (brain or spinal cord). Spasticity is often associated with conditions such as stroke, multiple sclerosis, cerebral palsy, spinal cord injury, and certain neurological disorders.
-also can b due to damage to motor cortex
what are tourettes? (hyperkinesia)
- due to damage to the basal ganglia: Damage to cells of the caudate nucleus
-Excessive movement
– involuntary tics, vocalizations
how can you treat Parkinson’s?
Treatment = not curative
- Physical therapy
-Medication, e.g. L-dopa = gold standard
-Deep Brain Stimulation (DBS)
split-brain
Hemianopia
Scotomas
-Small lesion within V1
Small receptive fields = small areas in the visual field
-Often unaware of it because of :
nystagmus (constant movement of the eye)
“filling in”
Cortical blindness,
Blindsight,
-lesions in V1 &V2
-Loss of vision in part of visual field
-ability to respond to visual stimuli that they report not consciously seeing.
-Still able to indicate the location, motion and color of objects
-Not able to detect form, identify the object
-Problems with reading and face recognition
-half of the word appears absent
-The edge of the page is in the blind field
Dissociation of form from motion and colour, info bypasses V1 via V2 or a pathway via superior colliculus and thalamus
Agnosia
-inability to combine individual visual impressions into complete patterns
-Inability to recognize
-Inability to draw or copy
monocular blindness
-Optic nerve (before chiasm) is damaged
– one eye loses vision
what are Gait Ataxia and Apendicular ataxia ?
-Gait Ataxia (midline cerebellum)
balance posture, eye movements, walking – drunk
-Apendicular ataxia (lateral cerebellum)
arm, hand and finger movements
Loss of timing – tapping a beat or judging length of an interval
Problems with combined movements
Problems in movement accuracy, adjustment to errors
e.g. finger – nose testing
bitemporal hemianopia
-Optic chiasm damage
– temporal fields
u basically can’t see your peripheral vision(the sides)
(right) nasal hemianopia
- you lose vision in ‘the middle right ‘ of ur vision\nasal field
Lateral chiasm is damaged
– medial/nasal fields
binasal injury= can’t see in the middle effect
honorariums hemianopia
Optic tract (after chiasm) lesion
– One visual field loses vision
quadrant-anopia
Optic radiations (partial) – after LGN injury
– One visual quadrant of the vision is loss
Macular sparing
-V1 damage
-One visual field with macular sparing
Object agnosia:
-Apperceptive agnosia: the inability to develop a perception of the structure of the object
Associative agnosia: is the inability to identify an object while percept is intact
Apperceptive agnosia:
Able to perceive elementary aspects of the stimulus (features such as lines or colours) but no integration into a meaningful image; -mostly caused by large bilateral or R-sided lesions
Associative agnosia:
-the inability to recognize an object despite normal perception
-Able to copy it, but not able to identify it
-object remains meaningless; probably problems with semantic categorization);
-generally associated with L-sided lesions of the ventral stream farther up the hierarchy (temporal lobe)
Prosopagnosia
-Inability to recognize faces
-Able to recognize facial features
-Bilateral damage in a region below the calcarine fissure at the temporal junction (Fusiform gyrus)
alexia
-inability to construct whole words from separate letters
-Inability to access word memory
-Left fusiform gyrus lesions
Visuospatial agnosia
-Unable to understand the spatial relationships of objects
-Topographical disorientation: inability to recognize landmarks that indicate direction
-Linked to facial agnosia
Asomatognosia
loss of knowledge or sense of one’s own body
what is extintion?
-Not able to see two identical objects, but able to see two different objects(agnosia)
-Not able to feel touch on both sides of the body
what is Astereognosis?
Not able to recognize an object by touch
Anosognosia
Unawareness of one’s own illness
Finger agnosia
Unable to point to or show their fingers
Balint syndrome
Bilateral dorsal parietal lesion
Combination of symptoms related to parietal lobe function
Full visual field an intact recognition and identification of objects and colour
Inability to fixate eyes on specific stimuli
Simult agnosia
Inability to see two objects
Optic ataxia
Problems with reaching under visual guidance
Optic ataxia
Problems with reaching under visual guidance
Simultagnosia
Inability to see two objects
Visual Neglect
Right dorsal parietal lesions
Neglect of sensory information in the contralateral (left) field
Visual, auditory, sensory
Two theories:
Defective integration of sensation into a percept.
Stimuli are perceived, but their location is uncertain and thus ignored.
Defective attention or orientation
No attention is directed to the left side
Defect in orienting to stimuli
Patient can learn to direct attention to the left
Acalculia
Difficulty performing mental arithmetic
Agraphia
(inability to write)
Writing upside-down and backwards
Apraxia
Movement disorder is characterized by the loss of skilled movement
Normal muscle tone, no muscle weakness, no tremor
Normal intellectual abilities and comprehension
Location:
Posterior parietal cortex and connection to frontal cortex
Ideomotor apraxia (left parietal cortex)
Inability to gesture or to copy series of movements
Copy series of facial movements
Constructional apraxia (right parietal cortex)
Inability to assemble a puzzle, constructing and draw in 2 or 3 dimensions
Auditory agnosia
a general inability to perceive
and identify complex sounds despite intact
hearing
Verbal auditory agnosia
-word deafness
* Can also result from subcortical damage to the auditory
tracts
