Final Neuro Flashcards

1
Q

Afferent neurons

A

Sensory

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2
Q

Efferent neuron

A

Motor

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3
Q

Brain coverings

A

Bony skill
Dura mater
Arachnoid membrane
Pia mater
(Need to know order)

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4
Q

Brain Cushioning

A

Subdural space
Subarachnoid space (contains CSF)

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5
Q

Cerebral Spinal Fluid

A

Serves as cushion
Baths brain with nutrients
Made in choroid plexus

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6
Q

Descending pathway

A

Brain to body
From motor cortex
Produces motor movement

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7
Q

Ascending pathway

A

Body to brain
To the sensory cortex
Produces sensation

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8
Q

Peripheral nerves

A

8 cervical
12 thoracic
5 lumbar
1 coccygeal

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9
Q

Cervical nerve roots

A

Named for the lower segment
Ex: C6 nerve root is at the C5-C6 nerve junction

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10
Q

Lumbar Nerve roots

A

Named for the upper segment
Ex: the L4 nerve root is located at the L4-L5 nerve junction

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11
Q

Autonomic Nervous System

A

Made up of the Sympathetic and Parasympathetic nervous systems

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12
Q

Anterolateral Afferent/Sensory Tract

A

Meant to be pleasurable
Controls pain, temp, crude vs light tough, itch, tickle, sexual sensation

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13
Q

Posterior Afferent/Sensory Tract

A

Meant to keep you alive
Controls position sense, discriminative touch, vibration sense, stereognosis, graphesthesia

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14
Q

Anatomy of anterolateral sensory tract

A

Small caliber axons
Unmyelinated or lightly myelinated -> slow conduction
Cell bodies in contraleral dorsal horn (crosses over and goes up/down cord)

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15
Q

Anatomy of posterior sensory tract

A

Large caliber axons
Heavily myelinated -> fast conduction
Cell bodies in ipsilateral dorsal horn (goes up same side that they enter/exit)

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16
Q

Efferent/Motor Tracts anatomy

A

Cell bodies in contralateral motor cortex
Fibers cross in pyramidal decussation (medulla)
Synapses with ipsilateral interneurons
Influences the activity of the lower motor neurons
Voluntary control of muscle movements

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17
Q

Cranial Nerve I

A

Olfactory nerve (S)
Smell

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18
Q

Cranial Nerve II

A

Optic nerve (S)
Vision

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19
Q

Cranial Nerve III

A

Oculomotor Nerve (M)
Upward, downward, medial eye movement, lid elevation and pupil constriction

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20
Q

Cranial Nerve IV

A

Trochlear Nerve (M)
Downward, medial eye movement

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21
Q

Cranial Nerve V

A

Trigeminal Nerve (S M)
Face, scalp, nasal mucosa, baccalaureate mucosa, (S)
Haw muscle, master muscle, temporal, digastric muscle (M)

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22
Q

Cranial Nerve VI

A

Abducens (M)
Lateral eye movement

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23
Q

Cranial Nerve VII

A

Facial nerve (S M)
External ear, taste front 2/3 tongue (S)
Facial movement, scalp, salivation, lacrimation (M)

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24
Q

Cranial Nerve VIII

A

Acoustic nerve (S)
Cochlear hearing

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25
Cranial Nerve IX
Glossopharyngeal (S M) External ear, back 1/3 tongue taste, carotid reflexes, sinus, baro and chemoreceptors (S) Gag, swallow, salivation (M)
26
Cranial Nerve X
Vagus (S M) External ear, pharynx (S) Swallow, pronation, bronchoconstriction, gastric secretion, peristalsis (M)
27
Cranial Nerve XI
Accessory (M) Swallow, pharyngeal muscles, head turn, shoulder rise
28
Cranial Nerve XII
Hypoglossal (M) Tongue muscle, hypoglossus
29
Mechanisms of injury
Hypoxic or ischemic injury Injury from excitatory AAs Increased volume and pressure Brain herniation Cerebral edema Hydrocephalus
30
Hypoxia
Deprivation of oxygen with maintained blood flow > depressant effects on the brain > euphoria, listlessness, drowsiness, impaired problem solving
31
Causes of hypoxia
Reduced atmospheric pressure Carbon monoxide poisoning Severe anemia Failure to oxygenate blood
32
Ischemia
Reduced or interrupted blood flow
33
Focal ischemia
When blood flow is inadequate to meet the metabolic demands of a part of the brain Stroke
34
Global ischemia
When blood flow is inadequate to meet the metabolic demands of the entire brain Needs immediate intervention Cardiac arrest or circulatory shock
35
Process of global ischemia
O2 is consumed in 10 seconds Glucose sources exhausted in 2-4 min Cellular ATP stores depleted in 4-5 min Excessive influx of sodium and calcium and efflux of potassium
36
Sodium and Calcium in Global Ischemia
Influx of sodium > neuronal and interstitial edema (carries water into the cells with it) Influx of calcium > “calcium cascade” release of intracellular and nuclear enzymes that cause cell destruction
37
Watershed zones
Global ischemic injuries occur here Blood vessels that supply two major regions Concentrated in anatomically vulnerable border zones between overlapping territories supplied by major cerebral arteries (middle, anterior, posterior)
38
Laminar necrosis
Global ischemic injury (Stroke) Occurs in areas supplied by the penetrating arteries - grey matter of the cerebral cortex Necrosis that develops in laminar (along a parallel plane or layer) and is most severe in the deeper layers of the cortex
39
Post Ischemic Hypoperfusion
Damage to blood vessels and changes in blood flow Prevents the return of adequate tissue perfusion despite reestablishment of circulation
40
Mechanisms involved in Post-Ischemic Hypoperfusion
Desaturation of venous blood Capillary and venous clotting Slugging of blood -> ^ blood viscosity -> ^ resistance to blood flow Immediate vasomotor paralysis d/t extracellular acidosis -> ischemic vasoconstriction Hypermetabolism d/t circulating catecholamines -> ^ cerebral metabolic rate and ^ need for energy producing substrates (now brain is in ^ demand of O2 and glucose AND isn’t perfusing well)
41
Treatment for global ischemia
Aimed at providing oxygen and decreasing metabolic needs during non-flow state
42
Methods of treatment for global ischemia
Decrease brain temp Normovolemic hemodilution to overcome slugging during reperfusion (give IV) Control of blood glucose 100-200 mg/mL
43
Excitotoxicity
Overstimulation of receptors for specific AAs that act as excitatory neurotransmitters (glutamate and aspartate)
44
Glutamate
Principle excitatory neurotransmitter in brain Activity is coupled with receptor-operated calcium ion channels -> calcium cascade
45
Glutamate role in injury
Injury > accumulation of extracellular glutamine > glutamate toxicity > initially (w/in minutes) neuronal swelling d/t sodium influx and later (w/in hours) effects f calcium cascade d/t calcium influx Accounts for long term effects of brain injury
46
Normal intracranial pressure (ICP)
5-15 mmHg
47
Confined Cavity Makeup
Blood volume (10%) + Brain tissue (80%) + CSF (10%)
48
Monroe-Kellie Hypothesis and Reciprocal Compensation
CSF and BV are the most able to compensate for changes in ICP If one increases another must decrease to make room for it
49
Causes of increased amounts of CSF
Excess production Decreased absorption Obstructed circulation
50
Causes of decreased amounts of CSF
Translocation to the spinal subarachnoid space or increased resorption
51
Causes of increased amounts of BV (Blood volume)
Vasodilation of cerebral blood vessels or obstruction of venous outflow
52
Causes of decreased amount of BV
Low pressure venous system has limited volume buffering capacity and blood flow controlled by autoregulatory mechanisms
53
Excessive intracranial pressure (ICP)
Obstructs cerebral blood flow Destroys brain cells (kills brain tissue) Displaces brain tissue (herniation)
54
Cerebral compliance
How much give you have in the fixed vault Compliance = change in volume / change in pressure
55
Pressure-Volume curve
Once compensatory mechanisms have been exceeded. Even small changes in volume result in dramatic increases in pressure
56
Cerebral Perfusion Pressure
Normal = 70-100 mmHg CPP = MABP (mean arterial BP) - ICP (intercranial pressure)
57
ICP ≥ MABP
Inadequate tissue perfusion, cellular hypoxia, neuronal death
58
Stage 1 of Intracranial Hypertension
Compensation ^ volume in one compartment -> decrease in one or both of other volumes Intracranial pressure remains near normal
59
Stage 2 of Intracranial Hypertension
Increase ICP Brain responds by constricting cerebral arteries to reduce pressure but results in hypoxia and hypercarbia and deterioration of brain function
60
Stage 3 of Intracranial Hypertension
Decompensation Cerebral arteries respond with reflex dilation -> ^ blood volume -> further increased ICP *small changes in intracranial volume result in large changes in pressure
61
Stage 4 of Intracranial Hypertension
Herniation or Loss of CPP Swelling and pressure -> herniation (only way brain can go is down into the brain stem) ICP = MABP -> no cerebral perfusion
62
Best sign of increased ICP
A decreased level if consciousness is the earliest and most reliable
63
Cushing reflex
CNS ischemic response triggered by ischemia of vasomotor center in brain - increased MABP - widening pulse pressure - reflex slowing of heart rate important by LATE indicator of increased intracranial pressure “Last ditch” effort to maintain cerebral circulation
64
Cerebral edema
Brain swelling - ^ tissue volume d/t abnormal accumulation - may or may not increase ICP Impact depends on the brain’s compensatory mechanisms and extent of swelling
65
Types of cerebral edema
Interstitial Vasogenic Cytotoxic
66
Interstitial Edema
Associated with an increase in sodium and water content of the peri-ventricular white matter Involves movement of CSF across ventricular wall Water and sodium pass into peri-ventricular white matter CONDITION: non communicating hydrocephalus
67
Vasogenic edema
Results from an increase in the ECF (extracellular fluid) that surrounds brain cells Brain injury > blood brain barrier disrupted > increased permeability and free diffusion across capillaries Can displace cerebral hemisphere and cause herniation
68
Where does Vasogenic edema occur
Occurs primarily in white matter b/c it is more compliant and offers less resistance to fluid accumulation than gray matter
69
Manifestation of Vasogenic edema
Focal neurologic deficits Disturbances in consciousness Severe intracranial HTN
70
Conditions that cause Vasogenic Edema
Tumors Prolonged ischemia Hemorrhage Brain injury Infectious processes that impair function of the blood brain barrier and allow transfer of water and protein into the interstitial space
71
Cytotoxic edema causes
Decreased blood flow > cellular hypoxia > decreased ATP production > decreased energy stores > decreased function of ion pumps > water entry and cellular swelling Decreased blood flow > cellular hypoxia > anaerobic metabolism > lactic acid and extracellular acidosis > water entry and cellular swelling
72
How cytotoxic edema causes death
Pre-synaptic hypo-polarization > opens voltage-gated calcium ion channels > increases levels free intracellular calcium > release of neurotransmitters > membrane potential to threshold > electrical hyperactivity (seizure) until exhaustion > electrical silence (death)
73
Cytotoxic edema
Involves actual swelling of brain cells Decreased An ^ in intracellular Slowly progressive process May be severe enough to rupture cells and produce cerebral infarction with necrosis of brain tissue
74
Where cytotoxic edema occurs
Primarily in the gray matter but may also be in white matter Can occur in vascular endothelium, smooth muscle cells, astrocytes, oligodendrocytes, or neurons
75
Manifestations of cytotoxic edema leads
Major changes, stupor, coma
76
Conditions associated with cytotoxic edema
Hypo-osmotic states such as water intoxication, severe ischemia that impairs sodium-potassium pump, hypoxia, acidosis, brain trauma
77
Treatment for cerebral edema
Does not necessarily disrupt brain function unless ^ ICP Localized edema surrounding brain tumors respond to corticosteroids, used in generalized edema controversial Stabilize cell membranes and scavenge free radicals Osmotic diuretics may be useful in an acute phase when hypoosmolarity is present
78
Confusion
Impaired ability to think clearly Inability to perceive, response to or remember current stimuli with customary repetition Disorientation
79
Delirium
Disturbed consciousness with motor restlessness Transient hallucinations Disorientation and sometimes delusion
80
Obtundation
Decreased alertness with psychomotor retardation
81
Stupor
Not unconscious but exhibits little or no spontaneous activity
82
Coma
Unarousable and unresponsive to external stimuli or internal needs Determined by Glasgow Coma Scale
83
Decorticate
Upper arms held tightly to sides with elbows, wrists, and fingers flexed Legs extended & internally rotated with feet plantar flexed
84
Decerebrate
Jaws clenched & neck extended Arms adducted & stiffly extended at elbows, with forearms pronated and wrists & fingers flexed Legs stiffly extended at knees with feet plantar flexed
85
Causes of decorticate posture
Destructive lesion of the corticospinal tracts within or very near cerebral hemisphere
86
Causes of decerebrate posture
Lesion in diencephalon, midbrain or pons Also may be caused by severe metabolic disorders such as hypoxia or hypoglycemia
87
Flaccidity
No motor response exhibited
88
Purposeful movement
Localizes to pain stimulus -> unconsciously attempts to remove painful stimulus
89
Complete flexion
Withdraws or flexes extremity indiscriminately in response to painful stimulus
90
Focal motor responses
Grasp reflex Sucking reflex Babinski reflex
91
Pupils are unequal or react sluggishly
Compression
92
Pinpoint or midpoint fixed pupils
Compression of brain stem
93
Dilated, fixed pupils
Compression of CN III
94
Unilateral, fixed pupils
Compression of one CN III
95
Oculomotor responses
Response means intakes brain stem No response > 48 hours means brain death
96
Oculocephalic reflex
(Doll’s eye response) Oculomotor response test Normal: when head turns side to side eyes rotate together to opposite side Abnormal: eyes rotate together in the same direction as the head
97
Oculovestibular reflex
(Cold or water caloric test) Oculomotor response test Normal: when ear canal irrigated with water eyes turn toward side being stimulated Abnormal: absence of eye movement
98
Cheyenne-stokes
Breathing pattern Alternating pattern of deep and shallow breathing with periods of apnea Common with diffuse cortical injury or coma from metabolic causes
99
Central neurogenic ventilation
Breathing pattern Regular hyperpneic pattern leads to decreased PCO2 and increased pH Common with increased ICP and structural damage to upper brain stem or cerebral cortex
100
Apneustic ventilation
Breathing pattern Prolonged inspirations cycle followed by a 2-3 sec paused, alternating with a prolonged expiratory cycle Found in lesions of lower pons
101
Cluster Breathing
Breathing pattern Clusters of breaths alternating with irregular periods of apnea Common Indicates damage to lower pons or high medulla
102
Ataxic breathing
Chaotic respiratory effort Indicates damage to the medullary respiratory control center
103
Hypo or hyperthermia
Hypothalamic or putuitary injuries or with head trauma
104
Cushing’s Triad
Increased SBP and decreased DBP (increased PP) and decreased HR Occurs with increased pressure on lower brain stem before herniation
105
Glasgow Coma Scale
Based on Eye Opening (E), Motor Response (M) and verbal Response (V) Score lower than 8 need to intibate
106
GCS Eye Opening
Spontaneous — 4 To call — 3 To pain — 2 None — 1
107
GCS Motor Response
Obeys commands — 6 Localizes pain stimulus — 5 Normal flexion (withdraw) — 4 Abnormal flexion (decorticate) — 3 Extension (decerebrate) — 2 None (flaccid) — 1
108
GCS Verbal Response
Oriented — 5 Confused conversation — 4 Inappropriate words — 3 Incomprehensible sounds — 2 None — 1
109
Arterial blood flow in cerebral circulation
2 internal carotids 2 vertebral arteries > basilar artery All form the circle of Willis
110
Venous blood flow in cerebral circulation
2 sets of veins - no valves, flow depends on gravity and pressure in venous sinuses > increase ICP - deep cerebral venous system - superficial cerebral veins 2 internal jugular veins
111
Cerebral arteries
Anterior cerebral artery Middle cerebral artery Posterior cerebral artery Anterior choroid artery Basilar artery
112
Regulation of cerebral blood flow
Through auto regulatory or local mechanisms that respond to metabolic needs
113
Regulation of deep cerebral blood flow
Auto-regulatory
114
Regulation of superficial cerebral blood flow
Sympathetic Responsible for vasospasm seen in cerebral aneurysm rupture
115
Metabolic factors affecting cerebral blood flow
Carbon dioxide concentration - more CO2 in your body the more blood flow to brain Hydrogen ion concentration (pH) - BUT extracellular acidosis also induces vasomotor paralysis Oxygen concentration - decreased oxygen increased blood flow
116
Stroke definition
“Brain attack” vascular disorder that injures brain tissue - Clinical syndrome consisting of a constellation of neurologic findings, sudden or rapid in onset, which persist for more than 24 hours and whose vascular origins are limited to thrombotic or embolism occlusion of a cerebral artery resulting in infarction or a spontaneous rupture of a vessel resulting in intracerebral or subarachnoid hemorrhage
117
Key aspects of a stroke
Pathological process affecting blood vessels that result in occlusion or rupture of blood vessels Resultant damage to brain tissue in area served by occulated or ruptured vessel Neurologic sequelae as a result of interrupted blood flow
118
Ischemic stroke
Most common type Caused by an interruption of blow flow in a cerebral vessel of thrombotic or embolism origin
119
Thrombotic origin
Most common cause of ischemic stroke At the site Plaque build up Increased calcium deposit
120
Embolic origin
Clot traveled there
121
Hemorrhagic stroke
Caused by bleeding into brain tissue d/t hypertension, aneurysms, AV malformation, head injury or blood dyscrasias Less common BUT higher fatality rate
122
AV malformation
Arteries and veins clustered and tangled so prone to bleeding and clots
123
Stroke aftermath
If you a stroke you are much more likely to have another stroke
124
Most important modifiable risk factor for stroke
Hypertension
125
Most common warning signs of stroke
Sudden numbness, weakness, or paralysis of the face, arm or leg, usually on one side of the body Loss of speech or trouble talking or understanding speech Sudden blurred or decreased vision usually in one eye Dizziness, loss of balance or loss of coordination Sudden severe headache with no apparent cause Difficulty swallowing
126
Bifurcation
Where the blood vessels split into two Most common spot for am embolism to land
127
Transient Ischemic Attack (TIA)
Type of ischemic stroke Characterized by focal ischemic cerebral neurologic deficits that last <24 hrs May provide warning of impending stroke Early diagnosis may permit early intervention and prevent extensive damage
128
Causes of TIA
Atherosclerotic disease and emboli
129
S/S of transient ischemic attack (TIA)
Depend on cerebral vessel involved Numbness and mild weakness on 1 side of body Forearm, hand and angle of mouth commonly affected Transient visual disturbances RARELY: isolated vertigo or dizziness, confusion, amnesia or seizures
130
TIA diagnosis
CT scan Cerebral vascular arterial imagining Cardiac imaging
131
TIA treatment
Depends on type and location Pharmacologic - aspirins, anti-platelet drugs, anticoagulants Avoidance of dehydration and hypotension Judicious use of meds to lower BP for HTN Surgery - removal of atherosclerotic plaques
132
Carotid endaterectomy
Surgical procedure if you have 1+ TIAs or mild strokes in the past 6 months and carotid stenosis Risk: cutting the vessel
133
Extracranial - intracranial bypass
Surgical procedure that redirects blood flow from an artery in the scalp through the cranium to cerebral arteries
134
Thrombotic Stroke
Most common cause of ischemic stroke Usually occur in atherosclerotic blood vessels - primarily at bifurcations Often accompanied by evidence of arteriosclerotic heart disease Not associated with activity Consciousness may or may not be lost Tend to occur in older people
135
Lacunar Infarcts
Ischemic stroke Small to very infarcts (holes) located in deeper noncortical parts of the brain or in the brain stem Results from occlusion of smaller branches of larger cerebral arteries In process of healing leave behind small cavities or “lacuna” Do not usually cause profound deficits
136
Most common sites for Lacunar Infarcts
Found in area of deep penetrating arteries supplying the internal capsule basal ganglia or brain stem Middle or posterior cerebral arteries
137
Causes of Lacunar Infarcts
Embolism Hypertension Small vessel occlusive disease Hematologist abnormalities Small intracerebral hemorrhages Vasospasm
138
Cardiogenic embolic stroke
Usually affects smaller cerebral vessels, often at bifurcations Sudden onset with immediate maximum deficit
139
Most common site of cardiogenic embolic stroke
Middle cerebral artery distribution * offers the path of least resistance
140
Predisposing conditions for cardiogenic embolic stroke
Rheumatic heart disease Arterial fibrillation Recent MI Ventricular aneurysm Bacterial endocarditis
141
Heart Disease and cardiogenic embolic stroke
Tx of HD decreases the incidence of embolic strokes
142
Ischemic Penumbra in evolving stroke
Central core of dead/dying cells Surrounded by ischemic area of minimally surviving cells = the “penumbra” (halo) Brains cells in it receive marginal blood flow, metabolism is altered and undergoes electrical failure BUT structural integrity of brain cells maintained
143
Survival after an ischemic stroke depends on
Return of adequate circulation Volume of toxic products released Degree of cerebral edema Alterations in local blood flow
144
Hemorrhagic Stroke
145
Hemorrhagic stoke 2
Rupture of a blood vessel and bleeding into the brain - edema - compression of brain contents - spasm of adjacent blood vessels
146
Most common predisposing factor of hemorrhagic stroke
Hypertension
147
Causes of hemorrhagic stroke
Aneurysm Spontaneous intracerebral hemorrhages AV malformations Other: trauma, erosion of the vessels by tumors, coagulopathies, vasculitis, drugs
148
Hemorrhagic stroke progression
Occurs suddenly, usually when person is active Vomiting common at onset, sometimes with headache Focal symptoms depend on which vessel is involved Hemorrhage into internal capsule > contralateral hemiplegia with initial flaccidity progressing to spasticity Clinical course often progresses rapidly to come and frequently to death
149
Acute manifestations of stroke
Specific manifestations determined by affected cerebral artery, area of brain supplied and adequacy of collateral circulation May include: Low of consciousness Cognitive and motor disorders Specific motor or sensory impairment Aphasia Hemi-neglect syndrome
150
Brain area involved in an occlusion in anterior cerebral artery
Infarction of medical aspect of 1 front lobe (if distal to communicating artery) Bilateral front infarction (if flow in other anterior cerebral arterial is inadequate
151
S/S occlusion in anterior cerebral artery
Paralysis of contralateral foot or leg Impaired gait Paresis of contralateral arm Contralateral sensory loss over toes, foot, and leg Problems making decisions or performing acts voluntarily Lack of spontaneity, easily distracted Slowness of thought Aphasia depends on the hemisphere involved Urinary incontinence Cognitive and effective disorders
152
Brain area involved in occlusions in the middle cerebral artery
Massive infarction of most of lateral hemisphere and deeper structures of the frontal, parietal and temporal lobes, internal capsule, basal ganglia
153
S/S of occlusion in the middle cerebral artery
Contralateral hemiplegia (face and arm) Contralateral sensory impairment Aphasia Homonymous hemianopsia Altered consciousness (confusion to coma) Inability to turn eyes toward paralyzed side Denial of paralyzed side or limb (hemi-attention) Possible acalculia (inability to perform calculations) Alexia (word blindness) Finger agnosia (inability to identify fingers) Left-right confusion Vasomotor paresis and instability
154
Brain area involved in posterior cerebral artery occlusion
Occipital lobe Anterior and medial portion of temporal lobe Thalamus involvement Cerebral peduncle involvement
155
S/S occlusion in the posterior cerebral artery altering the occipital love and anterior and medial portion of temporal lobe
Homonymous hemianopsia Color blindness Loss of central vision Visual hallucinations Memory deficits Preservation (repeated performance of same verbal or motor response)
156
S/S of occlusion of posterior cerebral artery affect thalamus involvement
Loss of all sensory modalities Spontaneous pain Intentional tremor Mild hemiparesis Aphasia
157
S/S of occlusion of posterior cerebral artery affecting cerebral peduncle involvement
Oculomotor nerve palsy with contralateral hemiplegia
158
S/S of occlusion of posterior cerebral artery affecting cerebellum and brain stem
Visual disturbance Diplopia (double visions) Dystaxia (shaky muscles) Vertigo Dysphasia (trouble swallowing) Dysphonia (trouble with vocal cords)
159
Stroke diagnosis
Complete Hx and Px with thorough neurologic exam Computed tomography (CT) Magnetic Resonance Imaging (MRI) Arteriography Magnetic resonance arterigraphy (MRA) Positron Emission Tomography (PET) Single-photon emission computed tomography (SPECT) Doppler ultrasound (US)
160
Stroke treatment
Emphasis on salvaging brain tissue and minimizing long term disability Education - do not wait for s/s to subside seek immediate treatment Early rehabilitation “Window of opportunity” for ischemic stroke - can use thrombolytic agents in early treatment Less dramatic treatment for hemorrhagic stroke
161
Thrombolytic agents
Can only use in “window of opportunity” first 3-4 hours in ischemic stroke Can’t be administered if: On anticoagulants GI bleed Recent MI, stroke or head injury Surgery in past 14 days High BP
162
Long term disabilities of strokes - motor deficits
After stroke affecting corticospinal tract > profound weakness on contralateral side Areas: motor cortex, posterior limp of internal capsule, medullary pyramids When muscle tone returns flaccidity s replaced by spasticity (6-8 weeks) > Passive range of motion
163
Long term disabilities of strokes - motor deficits Sx
Decrease/absence normal muscle tone Immediate loss of fine manipulative skills Affected limb tenses to move as whole > PROM
164
Long term disabilities of strokes - language
Involves higher order integrative functions of forebrain Used to communicate thought and feelings through use of symbolic formulations (words or numbers) Information is transmitted vocally (spoken) or visually (written)
165
Long term disabilities of strokes - speech
Involves mechanical act of articulating language = “motor act” of verbal expression Depends on functional integrity of peripheral musculature and its control
166
Long term disabilities of strokes - language and speech problems
Disturbances of the central processing mechanisms of language > aphasia Dysfunction of the larynx, pharynx, palate, tongue, lips and mouth > dysarthria Inability to sequence of voluntary movements needed for speech > apraxia
167
Long term disabilities of strokes -aphasia
Encompasses varying degrees of inability to comprehend, integrate and express language
168
Most common cause of aphasia
Middle cerebral artery of dominant hemisphere
169
Long term disabilities of strokes - receptive or fluent aphasia
Represents a sensory agnosia or inability to comprehend spoken words - may be visual or auditory Affected area: posterior temporal and lower parietal lobe
170
Long term disabilities of strokes - expressive or non fluent aphasia
Characterized by inability to translate thoughts or ideas into meaningful speech or writing Affected area: broca’a area of dominant frontal lobe
171
Dysarthria
Imperfect articulation of speech sounds or changes in voice pitch or quality Caused by disturbed motor control
172
Ataxia
Defective muscular coordination
173
Agnosia
Inability to recognize an object - may be tactile, visual, or auditory Involves structural damage to association centers of parietal, temporal and occipital lobes
174
Alexia
Word blindness
175
Anomia
Difficulty recognizing or naming objects or colors
176
Conduction aphasia
Inappropriate word use despite good comprehension Results from destruction of fibers connecting Wernicke’s and Broca’a areas
177
Neologisms
Invented words
178
Long term disabilities of strokes - denial or Hemi-attention
Inability to analyze and interpret sensory information and internal production of abnormal signals > denial of illness and denial of 1/2 body and surrounding environment Impaired spatial orientation Difficulty localizing stimuli, their own limbs and objects in space More common in strokes affecting non dominant side of brain (right hemisphere)
179
Right sided stroke
Weakness (hemiparesis) , paralysis (hemiplegia) or lack of coordination of the face arms or leg on the left side of the body Lack of feeling and position on the left side Decreased ability to judge distance, size, position, rate of movement and form Inability to think clearly Loss of awareness of forgetting objects on the left side (left sided neglect) Quick and impulsive behavior Difficulty drawing, dressing or following a map *these depend on which side of the brain is “dominant”
180
Left sided stroke
Weakness (hemiparesis), paralysis (hemiplegia) r lack of coordination of the face, arm or leg on the right side of body Lack of feeling and position on the right side Difficulty in speaking (slurred or distorted), listening, writing, reading, calculating with numbers or understanding what others say (aphasia) Behavior changes (slow, cautious, somewhat disorganized) Loss of awareness or forgetting objects on the right side *these depend on which side of the brain is “dominant”