Flashcards in Test 7 Deck (161):
1
Cerebellar hemispheres
Lateral hemispheres
Intermediate hemispheres
2
Superior cerebellar peduncle
-connects to rostral pons
-contains mostly efferent fibers
3
Middle cerebellar peduncle
-connects to pons
- contains mostly afferent fibers from cerebral cortex
4
Inferior cerebellar peduncles
-connects to cuadal pons/rostral medulla
-contains mostly afferent fibers from BS and SC
-contains efferent to vestibular nuclei and RF in brainstem
5
Cerebellum
-detects movement that deviates from the intended cortical command.
-smoothly coordinates ongoing movements
-contributes to motor planning
- receives massive amounts of sensory input about actual movement from the spinal cord cerebellar tracts
-integrates this sensory information and adjusts movement as necessary
6
Three major functions of the cerebellum:
1. Synergy of movement: groups movements for the performance of selective responses
2. Maintenance of Upright Posture: Body position in space
3. Maintenance of Tone: maintaining tone during muscle contraction
Also participates in speech articulation, respiratory movements, motor learning and possibly higher-order cognitive processes
7
Three functional regions of the cerebellum
Lateral hemispheres
Intermediate hemispheres
Vermis and flocculonodular lobe
8
Lateral hemisphere of cerebellum function
-motor planning for extremities
- lateral corticospinal tract
9
Intermediate hemisphere of the cerebellum function
-Function: distal limb coordination
-lateral corticospinal tract, rubrospinal tracts
10
Vermis and flocculonodular lobe of teh cerebellum function
- proximal limb and trunk coordination : anterior corticospinal tract, reticulospinal tract, vestibulospinal
-balance and vestibuloocular reflexes: medial longitudinal fasciculus
11
Input to cerebellar cortex:
-mossy fibers (excitatory)
- climbing fibers (excitatory)
—both synapse directly or indirectly on Purkinje cells. Inputs to ther cerebllar cortex also have collateral fibers that synapse on deep cerebellar nuclei
12
Output from cerebellar cortex:
Purkinje fibers (inhibitory)
-project to the deep cerebellar nuclei and/ or vestibular nuclei (excitatory)
13
Deep cerebellar nuclei serve as...
Serve as an on/off center for cerebellar output
14
What are the Deep cerebellar nuclei?
-Lateral to medial “Don’t Eat Greasy Foodds”
-Dentate: input from lateral hemisphere
-Emboliform: input from intermediate hemisphere
-Globase: input from intermediate hemisphere
-Fastigial: input from vermis
15
Vestibular nuclei
-Function in some ways like deep cerebellar nuclei
-input from inferior vermis and flocculonodular lobe
16
Main cerebellar output pathways
Lateral hemispheres- Dentate
Intermediate hemispheres- interposed
Vermis- fastigial
Inferior vermis and flocculonodular lobe - vestibular
17
Why do cerebellar lesions cause ipsilaterall deficits in coordination?
-Pathways from the cerebellum that influence the lateral motor systems and periphery are double crossed
- lesions of the vermis don’t cause unilateral deficits because medial moor systems influence bilateral proximal trunk musculature
18
Who sends input to the cerebellum?
-input to the cerebellum id from virtually all areas of the cerebral cortex, many sensory modalities, brainstem nuclei, and the SC
-corticopontine fibers
-input also from vestibular nuclei, RF nuclei, and inferior olivary nuclei
19
Corticopontine fibers
-fibers traveling from the cerebral cortex to the cerebellum
-synapse in pons, and then are called pontocerebellar fibers
20
Spinocerebellar pathways
-unconscious proprioception of limb movements : dorsal spinocerebellar tract (LE), cuneocerebellar tract (UE)
- unconscious information regarding activity of spinal interneurons, as well as spinal reflex circuits: ventral spinocerebellar tract (LE), rostral spinocerebellar (UE)
-each cerebellar hemisphere receives information from the ipsi limbs. Inputs either dont cross or are double crossed
21
Ataxia side of lesion
-ipsi to the side of the lesion
-b/c of reciprocal connection between cerebellum, brainstem, an other regions, ataxia may be seen with lesions in these other location as well
-uncoordinated movement. Disordered contractions of agonist and antagonist muscles and lack or normal coordination b/w movements at different joints. Movements have irregular, wavering course that consists of continuous overshooting and over correcting
22
Midline lesions of the cerebellum
-unsteady gait and eye movement abnormalities
23
Lesions lateral to the vermis of cerebellum
-limb ataxia
-
24
Three classic signs of cerebellar damage
“ANT”
Ataxia, nystagmus, and (intention) tremor (with movement)
Also could have: dysrhythmia, dysdiadochokinesia, dysmetria
- Vertigo, N/V, unsteadiness, slurred speech, HA
25
Dysrhythmia
abnormal timing
26
Dysdiasochokinesia
Abnormal rapid alternating movements
27
Dysmetria
Abnormal distance trajectory
28
UMN or LMN lesions interfering with cerebellum exam
-UMN: can cause slow, clumsy movements of extremities
-LMN: can cause weakness, tests requiring little strength can be helpful (precision finger tap)
29
Basal ganglia lesion affect with a cerebellar exam
-can cause slow, clumsy movements, and/or gait unsteadiness
30
Sensory ataxia affecting cerebellar exam
-severe loss of position sens
—sensory ataxia should improve with visual feedback
31
Truncal ataxia
-lesions of the vermis
-wide -based, unsteady “drunk-like” gait
-in severe cases, the patient may also have problems sitting w/o support
32
Appendicular ataxia
-lesions of the intermediate or lateral cerebellum
-uncoordinated movement of the extremities
Lesions can involve vermis and both hemispheres
-intention tremor, patient attempts to move limb toward a target, produces irregular, oscillating movements in multiple planes through the trajectory
33
Ipsilateral localization of ataxia
-lesions of the cerebellar hemispheres cause ipsilateral ataxia of the extremities
-truncal ataxia is a bilateral disorder
—
34
False localization of Ataxia
-Ataxia can be caused by lesions outside the cerebellar cortex that involve cerebellar input or output pathways
-cerebellar peduncles, pons, corticopontine fibers, etc
35
Most common tests for appendicular ataxia
-finger -nose-singer and heel-shin test
Watch for dysmetria and dysrhythmia
36
Most common tests for truncal ataxia
-tandem gait (heel-to-toe gait)
-Patients will tend to fall or sway to the side of the lesion if it extends slightly into a cerebellar hemisphere, as with ischemia
-Romber test: note increased sway or fall
37
Cerebellar artery infarcts S/S:
-limb ataxia, unsteady gait, nystagmus, vertigo, N/V, HA
38
SCA cerebellar infarcts
-SCA and PICA most common
- ipsi ataxia with little/no brainstem signs
-mostly involves the cerebellum itself and usually spares the lateral brainstem
39
PICA cerebellar infarcts
-SCA and PICA most common
- ipsi atacis, with nystagmus, vertigo, and N/V
-involves inferior cerebellar peduncle and vestibular nuclei
-also can see signs of lateral medullary (Wallenberg’s) syndrome
40
AICA cerebellar infarcts
-supplies internal auditory artery
-unilateral hearing loss
41
What can mimic S/S of cerebellar infarcts?
-infarcts to lateral pons or medulla because of cerebellar peduncles and vestibular nuclei involvment
42
What happens if the cerebellum swells?
Can cause hydrocephalous because compression of the 4th ventricle. As well as compression of vital brainstem structures and subsequent herniation
43
Amyotrophic lateral sclerosis (ALS)
-lou Gehrig's disease
-most common neuromuscular disease
-adult onset terminal disease of unknown cause
- characterized by the degeneration and scarring of neurons in the SC, brainstem (CST,CBT) and
-combination of both UMN and LMN resulting in limitation of movement
44
ALS etiology
-unknown, may be the result of multiple mechanisms that lead to neurodegeneration
- SODs-a group of enzymes that eliminate oxygen free radicals
-glutamate excitatory neuro transmitter can trigger a cascade of events leadingto cell death. inc levels in the CSF and plasma.
-clumping of neurofilament proteins
-lymphocytes are present which indicate immunoreactions
-environmental triggers
45
toxic theories for ALS
-related to lead or aluminum and abnormalities in magnesium and calcium levels
46
ALS pathophysiology
-massive loss of anterior horn cells of the SC and motor cranial nerve nuclei result in weakness and atrophy. greatest loss in Cervical and lumbar regions of the cord
-demyelination and gliosis of the CST and CBT
-Dementia
-reduce RNA in damaged cells
-accumulation of pigmented lipids
47
what is spared in patients with ALS?
- external ocular muscles III,IV,VI
-control of the muscles of the pelvic floor
- sensory systems and the spinocerebellar tracts are also generally spared
48
ALS diagnosis
-largely clinical
-criteria for diagnosis with EMG: spontaneous fibrillation and fasciculation in at least 3 limbs and the paraspinal muscles. these changes occur w/o any change in sensory response
-no single lab test but creatine phosphate levels are elevated in individuals with ALS
49
ALS clinical manifestation
-concomitant UMN and LMN sign in three spinal regions or two spinal regions with bulbar signs
-fasciculations: tongue, muscle crampls, stiffness, fatigue, weakness and atrophy.
hyper-refelxia, spasticity, positive Hoffman's and babinski
50
Pseudobulbar palsy
-reflects damage in the corticobulbar tract
51
progressive bulbar palsy
- cranial nerve nuclei involvement
-weakness in the muscles that control chewing swallowing and facial gestures
-dysarthria
52
Primary lateral sclerosis
-result of neuronal loss in the cortex
-CST involvement including hyperactive reflexes, weakness, and spasticity
53
Progressive Spinal muscular atrophy
-loss of motor neurons in th anterior horn cells of the SC
-weakness and wasting in the muscles of the cervical spine, hands with progression to other are of the body including facial symptoms and respiratory failure
54
ALS treatment
-Riluzole: inhibits glutamate release. appears to be neuroprotective to slow the disease but it is not curative
-Celastrol: strong anti-inflammatory and antioxidant that suppresses nitric oxide production
-tamoxafin: inhibit PKC which mediates inflammation
talampanel minocycline, memantine, myotrophin, coenzyme Q10, ketogenic diet
55
Alzheimer's dementia
-early in the disease coruse AD may have memory loss
-progressive aphasia or progressive apraxia
-decline in intellectual functioning severe enough tointerfere with personal relationships and an inability to carry out ADLs
56
Lewy Body disease
-progressive deterioration of cognition with no response to Parkinson's medication
-presence of lewy bodies found in neurofibrillary tangle and senile plaques
-characterized by asymmetrical gait, apraxia, rigidity and myoclonus
57
Alzheimer's : Pathology
-accumulation of insoluable material, amyloid. amyloid B protein is necessary t maintain fibroblasts and cell function. in AD the protein is not reabsorbed and tends to clump. when the clump contacts a neuron it destroys it
- loss of ACH and receptors
-glutaminergic neurons appear rpone to tangles
58
Alzheimer's treatment
-no cure for AD
- treatment focuses on detection, early administration of cholinesterase inhibitors and/or NMDA receptor targeted therapy.
-dietary changes
59
Multiple sclerosis
-named for sclerotic plaques that develop on CNS
-multiple lesions are found throughout the brain and SC and slow or block neural transmission resulting in weakness, sensory loss, and visual disturbances
60
MS : etiology
- unknown, family history
- human leukocyte antigen region on chromosome 6 has been identified as the one genetic determinant for MS which contributes to a small fraction fro the genetic basis for MS
-coexisting autoimmune disorders are seen in a majority of MS patients
61
MS: pathophysiology
-chronic inflammatory autoimmune, demyelinating disease of the CNS
- an abnormality in the immune response that results in an attack on the individual own neural tissue
-may be triggered by virus or infectious agent
-Tcel mediated causingthe overproduction of proinflammatory cytokines that recruit inflammatory cells.
62
relapsing -remitting MS
-relapses with full recovery or some remaining neurological symptoms and residual deficits.
63
Primary -progressive MS
disease progression from the onset w/o remission
64
secondary- progressive MS
initial relapsing-remitting course followed by progression at a variable rate
65
pregressive-relapsing MS
-progressive disease from onset but with clear acute relapses that may or may not have some recovery or remission
66
MS onset of S/S
-progressive disability over time
-great variability
-symptoms may develop quickly over minutes or hours or less commonly, slowly over several days or weeks
-optic neuritis is often the first manifestation of MS and usually presents unilaterally
-weakness and balance problems
67
Lhermitte's sign
-momentary electric shock like sensation evoked by neck flexion or cough and hea sensitivity which can cause a temporary increase in symp after exercise
-pain usually a burning neuropathic type
-trigeminal neuralgia may be present
68
MS bowel and bladder dysfunction
- bowel is less affected than bladder function
-irritable bowel is a common problem
-often there is dyssynergia between the bladder and the urinary sphincter
-urgency, frequency, an incontinence are associated with an overactive bladder
-sexual dysfunction present as well
69
MS: corticospinal Syndrome
-most common, involving CST and dorsla column
- stiffness, slowness, weakness, spasticity, +clonus, +Babinski
-paresthesias
70
MS: Brainstem syndrome
-lesions in CN nuclei III-XII
-S/S: gaze palsies, nystagmus, dysarthria
-vertigo may appear suddenly with gait unsteadiness and vomiting
-trigeminal neuralgia: shock like pain in the face
71
MS: CErebellar Syndrome
-may be symmetric with all 4 extremities or asymmetric with only one side
-ataxia
-hypotonia
-trunk weakness
-dysarthria
72
MS: cerebral syndrome
-depression and progressive cognitive dysfunction
-emotional lability
-emotional incontinence
-optic neuritis: unilateral vision loss with pain
73
MS: diagnosis
-largely clinical
-MRI of the brain and SC is critical with gasolinium to distinguish old and new lesions
74
MS medical management
-no cure for MS
-slowing the activated immune system
- Current drug therapy can diminish approx 1/3 of the attacks
-ABC drugs are used
-corticosteroids
-depression meds and sleep aids
-focal injections of botulism
-spasticity
75
ABC drugs
A - interferon beta 1a, Avonex
B- interferon beta 1b, betaseron
C- glatiramer acetate, copaxone
76
Parkinsons
-atrophy of the brain that produce abnormalities of basal ganglia function
-progressive disease characterized by : rigidity , bradykinesia, tremor and postural instability
77
PD: risk factors
-more years formal education increase PD
--smokers have a decr risk of PD
- high levels of exercise may lower PD risk
-exposures to toxins or infections
78
PD: pathophysiology
-lesions do not cause paralysis or weakness but rather a change that leads to loss of adaptive control, slowing of movement and poor coordination.
-depletion of 70-80% of dopamine is estimated to occur before there S/S
79
D1 configuration
-incr efficiency or decr the effect of cortical output to the striatum depending on the context of the desired movement
80
D2
-primarily decr the effect of cortical input to the striatum
81
Levodopa
metabolic precursor of dopamine that is able to cross the BBB and is able to raise the striatal dopamine levels in the BG
-deterioration of overall therapeutic effectiveness can be expected over time with a reported increase in motor complication of 10 % each yr
82
Parkinson's plus syndrome
-saily of neurological disorders that result from neuronal loss in diff components of the BG
-dopaminergic midbrain neurons affected like in PD but DO NOT respond to L-dopa
-absence of resting tremor
-early falls- cognitive impairments
83
Progressive supranuclear palsy
most common
-bradykinesia, gait freezing, apraxia, frequent falls, rigidity, vertical gaze palsy. usually involves more cognitive impairment that PD
84
Wilson's disease
-hepatolenticular degeneration caused by faulty copper metabolism where copper accumulates slowly in the liver and brain.
-toxic effects of copper lead to degeneration of the liver and the BG
-inherited as an autosomal dominant trait.
-increased absorption of copper
-diagnosis with a Fleisher ring
-dystonia, rigidity, and bradykinesia, festination of gait and tremors
-difficulty speaking and swallowing
85
Wilson disease treatment
Penicillamine which inhibits copper absorption
86
restless leg syndrome
-desire to move the extremities and is associated with paresthesias, motor restlessness, with worsening symptoms at rest
-there is relief with activity or sensory stimulation
-reduced iron stores in the substantia nigra
-no loss of dopaminergic neurons
87
dystonia
-sustained, involuntary muscle contractions in the extreme ranges of movement. co-contraction of both the agonist and antagonist
-reciprocal inhibition of the motor neurons.
-often exhibited as twisting or repetitive movements
-general dystonia- whole body
-focal dystonia - one joint
88
Secondary dystonia
-Is the result of damage or scarring to small areas of the brain and have been attributed to drug use, acute trauma, infections, tumors and demyelination diseases
89
cervical dystonia
-most common of the focal dystonias
-involuntary rotation and lateral flexion of the neck
-painful and leads to OA and hypertrophy of the SCM
90
blepharospasm
-uncontrolled blinking or closure of the eyelids fro seconds or hours
91
oromandibular dystonia
- face and jaw muscles contract causing grimaces and facial distortions
92
huntington's disease
-abnormalities of movement, personality disturbances and dementia, inherited as autosomal dominant trait
-hyperactivity of the BG circuitry. too much movement
93
Huntington's pathology
-cause is unknown
-ventricles are enlarged as a result of an atrophied BG
-selective degeneration of the neurons projecting from the striatum to the Substantia nigra.
-reduces the amt of GABA, ACH, and metenkephalin. leaving an abundance by comparison of dopamine and NE which cause excessive excitement
- "milkmaid's" sign
94
Huntington's treatment
- treatment is symptomatic
-most beneficial meds are to block dopamine neurotransmission
-high incidence of side effects such as tardive dyskinesia
95
tardive dyskinesia
- drug induced disorder
-choreathetoid and dystonic movements
-often irreversible.
96
What makes up the striatum?
Caudate
Putamen
97
What makes up the lenticular nucleus
Putamen
Globus pallidus
98
Basal ganglia function
-indirect influence on movement - via thalamus
-involved in Planning, initiation, and execution of movement
“PIE”
-also postural control, muscle tone, production of automatic movements
-Does NOT receive sensory input
99
Input nuclei to BG
- from cortex
-primarily the striatum
-also substantia nigra SNc
100
Output nuclei of BG
-to thalamus
-via the globus pallidus internus and substantia nigra
101
Direct pathway
-two pathways exist from input to output BG nuclei
-net effect: thalamus excitation, facilitating movement
-result is GO movement
-leads to disinhibition (less inhibition) of thalamus = increased movement
102
Indirect pathway of BG
-two pathways exist from input to output BG nuclei
-net effect: thalamus inhibition, inhibiting movement
- NO movement, slow it down, stop it.
-indirect pathway: leads to inhibition of thalamus= decreased movement
103
BG inhibition on thalamus
-thalamus tells the body to MOVE IT and GO! Output is excitatory o motor cortex
-BG inhibits the Thalamus: via GPi and SNr. Normal output at rest is some amt of inhibition on the thalamus.
-how much the thalamus is inhibited by theBG will determine if movement will occur or not.
-the cortex contributes to how much the BG inhibits thalamus via the direct and indirect pathways
104
Channels through the BG
-BG has other channels for different functions
-each passes through different pathways and projects to different regions of the frontal lobes and limbic system
—motor channel: movement
—oculomotor : eye movements
— prefrontal : cognitive processes
— limbic: emotions, motivational desires
105
Movement disorders
-abnormal movement caused by BG dysfunction is often referred to as dyskinesia
-common clinical findings associated with BG: akinesia, bradykinesia, rigidity
106
Rigidity in disorders
-increased, uniform resistance to passive movement of a limb throughout the entire ROM
-superimposed rachetlike jerkiness to passive movement of a limb
107
Involuntary movements in movement disorders
-dystonia: sustained contraction of agonist and antagonist
-athetosis: worm like
-chorea : rapid jerky
-ballismus: large amp sudden violent flailing
-tics: twitching
-myoclonus: cyclical,spasmodic alteration in muscle contraction and relaxation
108
Tremor
- rhythmic or semi-rhythmic oscillation movements
-resting tremor often seen with BG lesions
109
Parkinson’s disease pathways
-direct pathway more severely effected
-DA normally had an excitatory effect on direct pathway and an inhibitory effect on indirect pathway
—with the loss of DA, the result is an underactive direct pathway, and an overactive indirect pathway, which produces no/less movement
110
Huntington’s disease pathway
-indirect pathway more severely affected
-less/ no Enk released by sriatum
-the result is disinhibition of the thalamus which produces movement
111
What are the function of the association cortex?
-high-order sensory processing
-motor planning
-language processing and production
- visual-spatial orientation
-determining socially appropriate behavior
-“abstract thought”
112
Unimodal association cortex
-modality specific
-somatosensory, auditory, visual, and motor association cortex
-receives input predominately from primary sensory cortex of specific modality
113
Heteromodal association cortex
-higher-order
-has bidirectional connections with both motor and sensory association cortex of all modalities and with limbic cortex
—
114
Praxis
-skilled motor tasks for both right an dleft limbs are programmed mainly by. The dominant (~left) hemisphere
-lesions of the dominant hemisphere are commonly associated with apraxia
115
Left hemispheric function in Language
-language function depends predominantly on the left hemisphere
Certain areas of the temporal lobe are often 50% larger in teh left hemisphere
-left hemisphere is dominant for language of right handed individuals and over 60-70% of left handed individuals
-lesiosn to left language areas do cause language dysfunction in left handed. Individuals
116
Left hemispheric function in arithmetic ability
-detailed analytical abilities and skills
117
Right hemispheric function in visual-spatial analysis and spatial attention
-analysis an dattention to visual environment
-only the right hemisphere cause significant deficits in overall spatial analysis and attention
118
Right hemisheric function in prosody
-imparting the emotional significance to languge
-emotion conveyed bytone,rhythm, timing, enunciation, etc. Of voice
119
Right hemispheric function in musical ability
-musical perception
-learning and reproducing a tune
120
What happens when we hear a word and tehn repeat it aloud?
-auditory info reaches primary auditory cortex
-auditory info is then comprehended in wernicke’s area (22)
—sequences of sounds identified and comprehended
-sounds converted to meaningful words
121
Language production : Broca’s area
-wernicke’s and broca’s areas communicate with each other via teh arcuate fasciculus
- (44,45)
-motor programming of speech
-formulates sequences of sounds
-activates nearby oral of PMC
-words converted back to sounds
122
How does information travel when one is reading?
- visual info reaches the PVC
-processed in visual association cortex
-travels anteriorly to reach the language areas
—written language will project to wernicke’s are via angular gyrus
123
Non-dominant hemisphere contribution to language
-recognition and production of affective elements of speech
124
Lesions to non-dominant hemisphere affect on language
-difficulty in judging intended expression imparted by tone of other’s voice
- difficulty producing emotionally appropriate expression in one’s own voice
125
Aphasia
-impairment of language
-spoken and written language is affected
126
Dysarthria
-impairment of speech in which the mechnaism for speech is damaged
-can be caused by lesions in corticobulbar path, CN nuclei or nerves V, VII, IX, X and /or XII, the cerebellum, BG, or in the muscles involved in speech production
127
What is the most common cause of acute onset of aphasia
Cerebral infarct
128
Broca’s aphasia
-caused by lesions affecting Broca’s area and adjacent structures in the dominant frontal lobe
-impairment in language production
-speech is not fluent and slow
-writing and readin g aloud slow
- difficulty in naming and repeating phrases
-speech output is better with semiautomatic words or phrases
-prosody is absent
-comprehension is intact
-AKA nonfluent aphasia, expressive aphasia, and motor aphasia
129
Most common etiology of Broca’s aphasia
-infarct of L MCA
-superior division
130
Wernicke’s aphasia
-caused by lesion of wernicke’s area and adjacent structures in the dominant temporoparietal lobe
-impairment in language comprehension
-speech is meaningless
-paraphasic errors can be either innappropriate substitutions of a word for one of similar meaning
-writing and reading aloud also consists of fluent but meaningless, paraphasic errors
-normal fluency and prosody
-production is relatively intact
-impaired repetition often occurs due to the damage and from disconnection from Broca’s area
-AKA fluent, receptive, or sensory aphasia
131
Most common etiology of Wernicke’s aphasia
-infarct of L MCA inferior divisions
132
Global aphasia
-aphasias don’t always fit precisely into the categories of Broca’s or wernicke’s apahasia
- impaired fluency, impaired comprehension, and impaired repetition
133
A language exam usually consists of three parts:
-fluency, comprehension, and repetition
134
Most common etiology of global aphasia
-large left MCA infarcts (including superior and inferior artery divisions)
135
Anomia
-difficulty in recalling names or words
-mild or severe
- normal fluency, comprehension and normal repetition exists but with naming difficulties and occasional paraphasia
-subtle anomia can be sensitive indicator of language dysfunction: naminf is often impaired and often the last function to recover in language disorders
136
APraxia (ideomotor)
-disconnects exists between the idea of movement and its motor execution
-inability to carry out an action in response to verbal command, despite intact comprehension, motor and sensory pathways and coordination
-1/3 of patients with aphasia have some apraxia
-lesion of left frontal association cortex, particularly the premotor cortex and supplementary motor area
137
Spatial attention: normal condition
-left hemisphere responds to stimuli on the right,and the right hemisphere responds to stimuli on the left
- right hemisphere responds strongly to both left and right-sided stimuli, resulting in a very slight left attention bias
138
Spatial attention: right hemispheric lesion
-left hemisphere is still able to attend to right-sided stimuli, but here is a severe deficit in attention to left-sided stimuli
139
Spatial attention: left hemispheric lesion
-right hemisphere is still able to attend to right sided-stimuli, so there is a minimal or no deficit in attention to right sided-stimuli
140
Spatial analysis
-parietal association cortex is at the junction of the parietal, temporal and occipital lobes
-lesion particularly of teh right parietal association cortex can cause problems with spatial analysis
141
Hemineglect syndrome
-most often due to lesions of the right parietal or right frontal cortex
-profound neglect for teh contralateral half of the external world, and sometimes for eh contra half of the body
-sometimes with anosognosia: lack of awareness of the illness or that anything is wrong
-much more pronounced and lasts longer with right hemispheric lesions: milder forms can occur with left hemispheric lesions, although rare
-with large strokes, recovery can take weeks to months: Pts are prone to injuries and falls, some remain deficit in contra attention
142
Indication of hemineglect
-bumping into objects on one side
-prone toinjuries on one side
-ignoring food on one side of plate
-grooming on one side
-lack of movement of unilateral limbs
-being unaware of deficits
143
Four main types of testing that can evaluate different aspects of hemineglect syndrome
1. Sensory neglect
2. Motor-intentional neglect
3. Combination of sensory and motor neglect
4. Conceptual neglect
144
Sensory neglect
-pt will ignore sensory stimuli in contra hemispace
- normal primary sensation must first be established by testing each side alone
-tactile neglect is the most common
-pt is aksed if stimuli was on right, left, or both sides
145
Motor-intentional neglect
-pt wil perform no movements or fewer movements in the contralateral hemispace
-tested with eyes closed and intermixing commands to raise right arm/leg, left arm/leg or both
-can also be tested by askig pt to raise UE/LE opposite the one that was touched
146
Combined sensory and motor neglect
-pen and paper tests
-line bisection task or line cancellation task
-pt with neglect will be off midline to their noon-neglected side
-drawing: draw large clock with numbers, can have pt copy simple or complex figure
147
Conceptual neglect
-patients’ internal representaions of tehir ow bodies or of external world exhibit contra hemineglect
-anosognosia
148
Anosognosia
-striking lack of awareness of te illness or that anything is wrong
149
Anosodiaphoria
-aware of a severe deficit , but show no concern/distress
-right hemispheric lesion
150
Hemiasomatogosia
-Pts deny that half of their body belongs to them
-right hemispheric lesion
151
Agnosia
-inability to recognize objects when using a specific sense, even though the primary sensory cortex intact
152
Astereognosis
-inability to recognize objects by touch an dmanipulation
153
Visual agnosia
-inability to recognize objects by vision
154
Auditory agnosia
-inability to recognize types of sounds
155
Problems commonly seen with RIGHT hemispheric damage
-unaware of deficit (anosognosia) -overestimate abilities, impulsive, poor judgement
-hemineglect
-agnosia
-mania
-frequent mood changes
156
Commonly seen with LEFT hemispheric damage
-aware of deficits: cautious, slow hesistant, anxious
-aphasia
-apraxia
-depression
-disorgaanized
157
Frontal lobe functions
“RIO”
-Restraint: inhibition of inapprpriate behaviors
-Initiative: motivation to pursue pos or productive activities
-Order: capacity to correctly perform sequencing tasks and a variety of other cognitive operations
158
Prefrontal cortex
-largest part of frontal lobe
herteromodal association cortex
-many bidirectional connections for higher-order processes. Carry out the function of goal-oriented behavior and self -awareness
159
Frontal lobe dysfunction evidence can be obtained from:
- History: from family who know behavior
-behavior abnormalities: abulia, disinhibition, incontinence
-mental status: attention and memory tetsing, perseveration, word generation, abstract resoning
-presence of primitive reflexes, frontal gait abnormalities
160
Inferior occipitotemporal cortex
-“WHAT” stream of visual analysis
-processes color and form involved in object identification and recognition
—
161