conditions Flashcards

1
Q

what is Anencephaly? why is it important?

A

-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

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2
Q

What is Huntington’s disease?
(hyperkinesia)

A

-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:-

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3
Q

what does Parkinson’s disease consist of?
(hypokinesia )

A
  • 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.

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4
Q

what are negative and positive symptoms?

A

-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.

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5
Q

what is cognitive slowing?

A

-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)

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6
Q

what is Hemiparesis?

A

-weakness or partial paralysis that affects one side of the body
-usually due to damage in motor areas (M1)

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7
Q

what is Hemiplegia?

A

-paralysis or severe weakness that affects one entire side of the body
-damage to motor cortex (ex: M1)

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8
Q

what is Spasticity?

A
  • 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
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9
Q

what are tourettes? (hyperkinesia)

A
  • due to damage to the basal ganglia: Damage to cells of the caudate nucleus
    -Excessive movement
    – involuntary tics, vocalizations
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10
Q

how can you treat Parkinson’s?

A

Treatment = not curative
- Physical therapy
-Medication, e.g. L-dopa = gold standard
-Deep Brain Stimulation (DBS)

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11
Q

split-brain

A
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12
Q

Hemianopia

A
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13
Q

Scotomas

A

-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”

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14
Q

Cortical blindness,

A
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15
Q

Blindsight,

A

-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

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16
Q

Agnosia

A

-inability to combine individual visual impressions into complete patterns

-Inability to recognize
-Inability to draw or copy

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17
Q

monocular blindness

A

-Optic nerve (before chiasm) is damaged
– one eye loses vision

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18
Q

what are Gait Ataxia and Apendicular ataxia ?

A

-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

19
Q

bitemporal hemianopia

A

-Optic chiasm damage
– temporal fields
u basically can’t see your peripheral vision(the sides)

20
Q

(right) nasal hemianopia

A
  • 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
21
Q

honorariums hemianopia

A

Optic tract (after chiasm) lesion
– One visual field loses vision

22
Q

quadrant-anopia

A

Optic radiations (partial) – after LGN injury
– One visual quadrant of the vision is loss

23
Q

Macular sparing

A

-V1 damage
-One visual field with macular sparing

24
Q

Object agnosia:

A

-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

25
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
26
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)
27
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)
28
alexia
-inability to construct whole words from separate letters -Inability to access word memory -Left fusiform gyrus lesions
29
Visuospatial agnosia
-Unable to understand the spatial relationships of objects -Topographical disorientation: inability to recognize landmarks that indicate direction -Linked to facial agnosia
30
Asomatognosia
loss of knowledge or sense of one’s own body
31
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
32
what is Astereognosis?
Not able to recognize an object by touch
33
Anosognosia
Unawareness of one's own illness
34
Finger agnosia
Unable to point to or show their fingers
35
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
36
Optic ataxia
Problems with reaching under visual guidance
37
Simultagnosia
Inability to see two objects
38
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
39
Acalculia
Difficulty performing mental arithmetic
40
Agraphia
(inability to write) Writing upside-down and backwards
41
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
42
Auditory agnosia
a general inability to perceive and identify complex sounds despite intact hearing
43
Verbal auditory agnosia
-word deafness * Can also result from subcortical damage to the auditory tracts
44