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Patho > Final Neuro > Flashcards

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
Q

Cranial Nerve IX

A

Glossopharyngeal (S M)
External ear, back 1/3 tongue taste, carotid reflexes, sinus, baro and chemoreceptors (S)
Gag, swallow, salivation (M)

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26
Q

Cranial Nerve X

A

Vagus (S M)
External ear, pharynx (S)
Swallow, pronation, bronchoconstriction, gastric secretion, peristalsis (M)

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27
Q

Cranial Nerve XI

A

Accessory (M)
Swallow, pharyngeal muscles, head turn, shoulder rise

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28
Q

Cranial Nerve XII

A

Hypoglossal (M)
Tongue muscle, hypoglossus

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29
Q

Mechanisms of injury

A

Hypoxic or ischemic injury
Injury from excitatory AAs
Increased volume and pressure
Brain herniation
Cerebral edema
Hydrocephalus

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30
Q

Hypoxia

A

Deprivation of oxygen with maintained blood flow > depressant effects on the brain > euphoria, listlessness, drowsiness, impaired problem solving

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31
Q

Causes of hypoxia

A

Reduced atmospheric pressure
Carbon monoxide poisoning
Severe anemia
Failure to oxygenate blood

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32
Q

Ischemia

A

Reduced or interrupted blood flow

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33
Q

Focal ischemia

A

When blood flow is inadequate to meet the metabolic demands of a part of the brain
Stroke

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34
Q

Global ischemia

A

When blood flow is inadequate to meet the metabolic demands of the entire brain
Needs immediate intervention
Cardiac arrest or circulatory shock

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35
Q

Process of global ischemia

A

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

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36
Q

Sodium and Calcium in Global Ischemia

A

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

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37
Q

Watershed zones

A

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)

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38
Q

Laminar necrosis

A

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

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39
Q

Post Ischemic Hypoperfusion

A

Damage to blood vessels and changes in blood flow
Prevents the return of adequate tissue perfusion despite reestablishment of circulation

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40
Q

Mechanisms involved in Post-Ischemic Hypoperfusion

A

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)

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41
Q

Treatment for global ischemia

A

Aimed at providing oxygen and decreasing metabolic needs during non-flow state

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42
Q

Methods of treatment for global ischemia

A

Decrease brain temp
Normovolemic hemodilution to overcome slugging during reperfusion (give IV)
Control of blood glucose 100-200 mg/mL

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43
Q

Excitotoxicity

A

Overstimulation of receptors for specific AAs that act as excitatory neurotransmitters (glutamate and aspartate)

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44
Q

Glutamate

A

Principle excitatory neurotransmitter in brain
Activity is coupled with receptor-operated calcium ion channels -> calcium cascade

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45
Q

Glutamate role in injury

A

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

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46
Q

Normal intracranial pressure (ICP)

A

5-15 mmHg

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47
Q

Confined Cavity Makeup

A

Blood volume (10%) + Brain tissue (80%) + CSF (10%)

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48
Q

Monroe-Kellie Hypothesis and Reciprocal Compensation

A

CSF and BV are the most able to compensate for changes in ICP
If one increases another must decrease to make room for it

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49
Q

Causes of increased amounts of CSF

A

Excess production
Decreased absorption
Obstructed circulation

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50
Q

Causes of decreased amounts of CSF

A

Translocation to the spinal subarachnoid space or increased resorption

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51
Q

Causes of increased amounts of BV (Blood volume)

A

Vasodilation of cerebral blood vessels or obstruction of venous outflow

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52
Q

Causes of decreased amount of BV

A

Low pressure venous system has limited volume buffering capacity and blood flow controlled by autoregulatory mechanisms

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53
Q

Excessive intracranial pressure (ICP)

A

Obstructs cerebral blood flow
Destroys brain cells (kills brain tissue)
Displaces brain tissue (herniation)

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54
Q

Cerebral compliance

A

How much give you have in the fixed vault
Compliance = change in volume / change in pressure

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55
Q

Pressure-Volume curve

A

Once compensatory mechanisms have been exceeded. Even small changes in volume result in dramatic increases in pressure

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56
Q

Cerebral Perfusion Pressure

A

Normal = 70-100 mmHg
CPP = MABP (mean arterial BP) - ICP (intercranial pressure)

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57
Q

ICP ≥ MABP

A

Inadequate tissue perfusion, cellular hypoxia, neuronal death

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58
Q

Stage 1 of Intracranial Hypertension

A

Compensation
^ volume in one compartment -> decrease in one or both of other volumes
Intracranial pressure remains near normal

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59
Q

Stage 2 of Intracranial Hypertension

A

Increase ICP
Brain responds by constricting cerebral arteries to reduce pressure but results in hypoxia and hypercarbia and deterioration of brain function

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60
Q

Stage 3 of Intracranial Hypertension

A

Decompensation
Cerebral arteries respond with reflex dilation -> ^ blood volume -> further increased ICP
*small changes in intracranial volume result in large changes in pressure

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61
Q

Stage 4 of Intracranial Hypertension

A

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

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62
Q

Best sign of increased ICP

A

A decreased level if consciousness is the earliest and most reliable

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63
Q

Cushing reflex

A

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

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64
Q

Cerebral edema

A

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

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65
Q

Types of cerebral edema

A

Interstitial
Vasogenic
Cytotoxic

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66
Q

Interstitial Edema

A

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

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67
Q

Vasogenic edema

A

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

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68
Q

Where does Vasogenic edema occur

A

Occurs primarily in white matter b/c it is more compliant and offers less resistance to fluid accumulation than gray matter

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69
Q

Manifestation of Vasogenic edema

A

Focal neurologic deficits
Disturbances in consciousness
Severe intracranial HTN

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70
Q

Conditions that cause Vasogenic Edema

A

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

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71
Q

Cytotoxic edema causes

A

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

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72
Q

How cytotoxic edema causes death

A

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)

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73
Q

Cytotoxic edema

A

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
Q

Where cytotoxic edema occurs

A

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
Q

Manifestations of cytotoxic edema leads

A

Major changes, stupor, coma

76
Q

Conditions associated with cytotoxic edema

A

Hypo-osmotic states such as water intoxication, severe ischemia that impairs sodium-potassium pump, hypoxia, acidosis, brain trauma

77
Q

Treatment for cerebral edema

A

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
Q

Confusion

A

Impaired ability to think clearly
Inability to perceive, response to or remember current stimuli with customary repetition
Disorientation

79
Q

Delirium

A

Disturbed consciousness with motor restlessness
Transient hallucinations
Disorientation and sometimes delusion

80
Q

Obtundation

A

Decreased alertness with psychomotor retardation

81
Q

Stupor

A

Not unconscious but exhibits little or no spontaneous activity

82
Q

Coma

A

Unarousable and unresponsive to external stimuli or internal needs
Determined by Glasgow Coma Scale

83
Q

Decorticate

A

Upper arms held tightly to sides with elbows, wrists, and fingers flexed
Legs extended & internally rotated with feet plantar flexed

84
Q

Decerebrate

A

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
Q

Causes of decorticate posture

A

Destructive lesion of the corticospinal tracts within or very near cerebral hemisphere

86
Q

Causes of decerebrate posture

A

Lesion in diencephalon, midbrain or pons
Also may be caused by severe metabolic disorders such as hypoxia or hypoglycemia

87
Q

Flaccidity

A

No motor response exhibited

88
Q

Purposeful movement

A

Localizes to pain stimulus -> unconsciously attempts to remove painful stimulus

89
Q

Complete flexion

A

Withdraws or flexes extremity indiscriminately in response to painful stimulus

90
Q

Focal motor responses

A

Grasp reflex
Sucking reflex
Babinski reflex

91
Q

Pupils are unequal or react sluggishly

A

Compression

92
Q

Pinpoint or midpoint fixed pupils

A

Compression of brain stem

93
Q

Dilated, fixed pupils

A

Compression of CN III

94
Q

Unilateral, fixed pupils

A

Compression of one CN III

95
Q

Oculomotor responses

A

Response means intakes brain stem
No response > 48 hours means brain death

96
Q

Oculocephalic reflex

A

(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
Q

Oculovestibular reflex

A

(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
Q

Cheyenne-stokes

A

Breathing pattern
Alternating pattern of deep and shallow breathing with periods of apnea
Common with diffuse cortical injury or coma from metabolic causes

99
Q

Central neurogenic ventilation

A

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
Q

Apneustic ventilation

A

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
Q

Cluster Breathing

A

Breathing pattern
Clusters of breaths alternating with irregular periods of apnea Common
Indicates damage to lower pons or high medulla

102
Q

Ataxic breathing

A

Chaotic respiratory effort
Indicates damage to the medullary respiratory control center

103
Q

Hypo or hyperthermia

A

Hypothalamic or putuitary injuries or with head trauma

104
Q

Cushing’s Triad

A

Increased SBP and decreased DBP (increased PP) and decreased HR
Occurs with increased pressure on lower brain stem before herniation

105
Q

Glasgow Coma Scale

A

Based on Eye Opening (E), Motor Response (M) and verbal Response (V)
Score lower than 8 need to intibate

106
Q

GCS Eye Opening

A

Spontaneous — 4
To call — 3
To pain — 2
None — 1

107
Q

GCS Motor Response

A

Obeys commands — 6
Localizes pain stimulus — 5
Normal flexion (withdraw) — 4
Abnormal flexion (decorticate) — 3
Extension (decerebrate) — 2
None (flaccid) — 1

108
Q

GCS Verbal Response

A

Oriented — 5
Confused conversation — 4
Inappropriate words — 3
Incomprehensible sounds — 2
None — 1

109
Q

Arterial blood flow in cerebral circulation

A

2 internal carotids
2 vertebral arteries > basilar artery
All form the circle of Willis

110
Q

Venous blood flow in cerebral circulation

A

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
Q

Cerebral arteries

A

Anterior cerebral artery
Middle cerebral artery
Posterior cerebral artery
Anterior choroid artery
Basilar artery

112
Q

Regulation of cerebral blood flow

A

Through auto regulatory or local mechanisms that respond to metabolic needs

113
Q

Regulation of deep cerebral blood flow

A

Auto-regulatory

114
Q

Regulation of superficial cerebral blood flow

A

Sympathetic
Responsible for vasospasm seen in cerebral aneurysm rupture

115
Q

Metabolic factors affecting cerebral blood flow

A

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
Q

Stroke definition

A

“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
Q

Key aspects of a stroke

A

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
Q

Ischemic stroke

A

Most common type
Caused by an interruption of blow flow in a cerebral vessel of thrombotic or embolism origin

119
Q

Thrombotic origin

A

Most common cause of ischemic stroke
At the site
Plaque build up
Increased calcium deposit

120
Q

Embolic origin

A

Clot traveled there

121
Q

Hemorrhagic stroke

A

Caused by bleeding into brain tissue d/t hypertension, aneurysms, AV malformation, head injury or blood dyscrasias
Less common BUT higher fatality rate

122
Q

AV malformation

A

Arteries and veins clustered and tangled so prone to bleeding and clots

123
Q

Stroke aftermath

A

If you a stroke you are much more likely to have another stroke

124
Q

Most important modifiable risk factor for stroke

A

Hypertension

125
Q

Most common warning signs of stroke

A

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
Q

Bifurcation

A

Where the blood vessels split into two
Most common spot for am embolism to land

127
Q

Transient Ischemic Attack (TIA)

A

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
Q

Causes of TIA

A

Atherosclerotic disease and emboli

129
Q

S/S of transient ischemic attack (TIA)

A

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
Q

TIA diagnosis

A

CT scan
Cerebral vascular arterial imagining
Cardiac imaging

131
Q

TIA treatment

A

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
Q

Carotid endaterectomy

A

Surgical procedure if you have 1+ TIAs or mild strokes in the past 6 months and carotid stenosis
Risk: cutting the vessel

133
Q

Extracranial - intracranial bypass

A

Surgical procedure that redirects blood flow from an artery in the scalp through the cranium to cerebral arteries

134
Q

Thrombotic Stroke

A

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
Q

Lacunar Infarcts

A

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
Q

Most common sites for Lacunar Infarcts

A

Found in area of deep penetrating arteries supplying the internal capsule basal ganglia or brain stem
Middle or posterior cerebral arteries

137
Q

Causes of Lacunar Infarcts

A

Embolism
Hypertension
Small vessel occlusive disease
Hematologist abnormalities
Small intracerebral hemorrhages
Vasospasm

138
Q

Cardiogenic embolic stroke

A

Usually affects smaller cerebral vessels, often at bifurcations
Sudden onset with immediate maximum deficit

139
Q

Most common site of cardiogenic embolic stroke

A

Middle cerebral artery distribution * offers the path of least resistance

140
Q

Predisposing conditions for cardiogenic embolic stroke

A

Rheumatic heart disease
Arterial fibrillation
Recent MI
Ventricular aneurysm
Bacterial endocarditis

141
Q

Heart Disease and cardiogenic embolic stroke

A

Tx of HD decreases the incidence of embolic strokes

142
Q

Ischemic Penumbra in evolving stroke

A

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
Q

Survival after an ischemic stroke depends on

A

Return of adequate circulation
Volume of toxic products released
Degree of cerebral edema
Alterations in local blood flow

144
Q

Hemorrhagic Stroke

A
145
Q

Hemorrhagic stoke 2

A

Rupture of a blood vessel and bleeding into the brain
- edema
- compression of brain contents
- spasm of adjacent blood vessels

146
Q

Most common predisposing factor of hemorrhagic stroke

A

Hypertension

147
Q

Causes of hemorrhagic stroke

A

Aneurysm
Spontaneous intracerebral hemorrhages
AV malformations
Other: trauma, erosion of the vessels by tumors, coagulopathies, vasculitis, drugs

148
Q

Hemorrhagic stroke progression

A

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
Q

Acute manifestations of stroke

A

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
Q

Brain area involved in an occlusion in anterior cerebral artery

A

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
Q

S/S occlusion in anterior cerebral artery

A

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
Q

Brain area involved in occlusions in the middle cerebral artery

A

Massive infarction of most of lateral hemisphere and deeper structures of the frontal, parietal and temporal lobes, internal capsule, basal ganglia

153
Q

S/S of occlusion in the middle cerebral artery

A

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
Q

Brain area involved in posterior cerebral artery occlusion

A

Occipital lobe
Anterior and medial portion of temporal lobe
Thalamus involvement
Cerebral peduncle involvement

155
Q

S/S occlusion in the posterior cerebral artery altering the occipital love and anterior and medial portion of temporal lobe

A

Homonymous hemianopsia
Color blindness
Loss of central vision
Visual hallucinations
Memory deficits
Preservation (repeated performance of same verbal or motor response)

156
Q

S/S of occlusion of posterior cerebral artery affect thalamus involvement

A

Loss of all sensory modalities
Spontaneous pain
Intentional tremor
Mild hemiparesis
Aphasia

157
Q

S/S of occlusion of posterior cerebral artery affecting cerebral peduncle involvement

A

Oculomotor nerve palsy with contralateral hemiplegia

158
Q

S/S of occlusion of posterior cerebral artery affecting cerebellum and brain stem

A

Visual disturbance
Diplopia (double visions)
Dystaxia (shaky muscles)
Vertigo
Dysphasia (trouble swallowing)
Dysphonia (trouble with vocal cords)

159
Q

Stroke diagnosis

A

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
Q

Stroke treatment

A

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
Q

Thrombolytic agents

A

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
Q

Long term disabilities of strokes - motor deficits

A

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
Q

Long term disabilities of strokes - motor deficits Sx

A

Decrease/absence normal muscle tone
Immediate loss of fine manipulative skills
Affected limb tenses to move as whole > PROM

164
Q

Long term disabilities of strokes - language

A

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
Q

Long term disabilities of strokes - speech

A

Involves mechanical act of articulating language = “motor act” of verbal expression
Depends on functional integrity of peripheral musculature and its control

166
Q

Long term disabilities of strokes - language and speech problems

A

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
Q

Long term disabilities of strokes -aphasia

A

Encompasses varying degrees of inability to comprehend, integrate and express language

168
Q

Most common cause of aphasia

A

Middle cerebral artery of dominant hemisphere

169
Q

Long term disabilities of strokes - receptive or fluent aphasia

A

Represents a sensory agnosia or inability to comprehend spoken words - may be visual or auditory
Affected area: posterior temporal and lower parietal lobe

170
Q

Long term disabilities of strokes - expressive or non fluent aphasia

A

Characterized by inability to translate thoughts or ideas into meaningful speech or writing
Affected area: broca’a area of dominant frontal lobe

171
Q

Dysarthria

A

Imperfect articulation of speech sounds or changes in voice pitch or quality
Caused by disturbed motor control

172
Q

Ataxia

A

Defective muscular coordination

173
Q

Agnosia

A

Inability to recognize an object - may be tactile, visual, or auditory
Involves structural damage to association centers of parietal, temporal and occipital lobes

174
Q

Alexia

A

Word blindness

175
Q

Anomia

A

Difficulty recognizing or naming objects or colors

176
Q

Conduction aphasia

A

Inappropriate word use despite good comprehension
Results from destruction of fibers connecting Wernicke’s and Broca’a areas

177
Q

Neologisms

A

Invented words

178
Q

Long term disabilities of strokes - denial or Hemi-attention

A

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
Q

Right sided stroke

A

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
Q

Left sided stroke

A

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”

Patho (6 decks)

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