Final Neuro Flashcards
Afferent neurons
Sensory
Efferent neuron
Motor
Brain coverings
Bony skill
Dura mater
Arachnoid membrane
Pia mater
(Need to know order)
Brain Cushioning
Subdural space
Subarachnoid space (contains CSF)
Cerebral Spinal Fluid
Serves as cushion
Baths brain with nutrients
Made in choroid plexus
Descending pathway
Brain to body
From motor cortex
Produces motor movement
Ascending pathway
Body to brain
To the sensory cortex
Produces sensation
Peripheral nerves
8 cervical
12 thoracic
5 lumbar
1 coccygeal
Cervical nerve roots
Named for the lower segment
Ex: C6 nerve root is at the C5-C6 nerve junction
Lumbar Nerve roots
Named for the upper segment
Ex: the L4 nerve root is located at the L4-L5 nerve junction
Autonomic Nervous System
Made up of the Sympathetic and Parasympathetic nervous systems
Anterolateral Afferent/Sensory Tract
Meant to be pleasurable
Controls pain, temp, crude vs light tough, itch, tickle, sexual sensation
Posterior Afferent/Sensory Tract
Meant to keep you alive
Controls position sense, discriminative touch, vibration sense, stereognosis, graphesthesia
Anatomy of anterolateral sensory tract
Small caliber axons
Unmyelinated or lightly myelinated -> slow conduction
Cell bodies in contraleral dorsal horn (crosses over and goes up/down cord)
Anatomy of posterior sensory tract
Large caliber axons
Heavily myelinated -> fast conduction
Cell bodies in ipsilateral dorsal horn (goes up same side that they enter/exit)
Efferent/Motor Tracts anatomy
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
Cranial Nerve I
Olfactory nerve (S)
Smell
Cranial Nerve II
Optic nerve (S)
Vision
Cranial Nerve III
Oculomotor Nerve (M)
Upward, downward, medial eye movement, lid elevation and pupil constriction
Cranial Nerve IV
Trochlear Nerve (M)
Downward, medial eye movement
Cranial Nerve V
Trigeminal Nerve (S M)
Face, scalp, nasal mucosa, baccalaureate mucosa, (S)
Haw muscle, master muscle, temporal, digastric muscle (M)
Cranial Nerve VI
Abducens (M)
Lateral eye movement
Cranial Nerve VII
Facial nerve (S M)
External ear, taste front 2/3 tongue (S)
Facial movement, scalp, salivation, lacrimation (M)
Cranial Nerve VIII
Acoustic nerve (S)
Cochlear hearing
Cranial Nerve IX
Glossopharyngeal (S M)
External ear, back 1/3 tongue taste, carotid reflexes, sinus, baro and chemoreceptors (S)
Gag, swallow, salivation (M)
Cranial Nerve X
Vagus (S M)
External ear, pharynx (S)
Swallow, pronation, bronchoconstriction, gastric secretion, peristalsis (M)
Cranial Nerve XI
Accessory (M)
Swallow, pharyngeal muscles, head turn, shoulder rise
Cranial Nerve XII
Hypoglossal (M)
Tongue muscle, hypoglossus
Mechanisms of injury
Hypoxic or ischemic injury
Injury from excitatory AAs
Increased volume and pressure
Brain herniation
Cerebral edema
Hydrocephalus
Hypoxia
Deprivation of oxygen with maintained blood flow > depressant effects on the brain > euphoria, listlessness, drowsiness, impaired problem solving
Causes of hypoxia
Reduced atmospheric pressure
Carbon monoxide poisoning
Severe anemia
Failure to oxygenate blood
Ischemia
Reduced or interrupted blood flow
Focal ischemia
When blood flow is inadequate to meet the metabolic demands of a part of the brain
Stroke
Global ischemia
When blood flow is inadequate to meet the metabolic demands of the entire brain
Needs immediate intervention
Cardiac arrest or circulatory shock
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
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
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)
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
Post Ischemic Hypoperfusion
Damage to blood vessels and changes in blood flow
Prevents the return of adequate tissue perfusion despite reestablishment of circulation
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)
Treatment for global ischemia
Aimed at providing oxygen and decreasing metabolic needs during non-flow state
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
Excitotoxicity
Overstimulation of receptors for specific AAs that act as excitatory neurotransmitters (glutamate and aspartate)
Glutamate
Principle excitatory neurotransmitter in brain
Activity is coupled with receptor-operated calcium ion channels -> calcium cascade
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
Normal intracranial pressure (ICP)
5-15 mmHg
Confined Cavity Makeup
Blood volume (10%) + Brain tissue (80%) + CSF (10%)
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
Causes of increased amounts of CSF
Excess production
Decreased absorption
Obstructed circulation
Causes of decreased amounts of CSF
Translocation to the spinal subarachnoid space or increased resorption
Causes of increased amounts of BV (Blood volume)
Vasodilation of cerebral blood vessels or obstruction of venous outflow
Causes of decreased amount of BV
Low pressure venous system has limited volume buffering capacity and blood flow controlled by autoregulatory mechanisms
Excessive intracranial pressure (ICP)
Obstructs cerebral blood flow
Destroys brain cells (kills brain tissue)
Displaces brain tissue (herniation)
Cerebral compliance
How much give you have in the fixed vault
Compliance = change in volume / change in pressure
Pressure-Volume curve
Once compensatory mechanisms have been exceeded. Even small changes in volume result in dramatic increases in pressure
Cerebral Perfusion Pressure
Normal = 70-100 mmHg
CPP = MABP (mean arterial BP) - ICP (intercranial pressure)
ICP ≥ MABP
Inadequate tissue perfusion, cellular hypoxia, neuronal death
Stage 1 of Intracranial Hypertension
Compensation
^ volume in one compartment -> decrease in one or both of other volumes
Intracranial pressure remains near normal
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
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
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
Best sign of increased ICP
A decreased level if consciousness is the earliest and most reliable
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
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
Types of cerebral edema
Interstitial
Vasogenic
Cytotoxic
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
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
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
Manifestation of Vasogenic edema
Focal neurologic deficits
Disturbances in consciousness
Severe intracranial HTN
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
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
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)
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
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
Manifestations of cytotoxic edema leads
Major changes, stupor, coma
Conditions associated with cytotoxic edema
Hypo-osmotic states such as water intoxication, severe ischemia that impairs sodium-potassium pump, hypoxia, acidosis, brain trauma
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
Confusion
Impaired ability to think clearly
Inability to perceive, response to or remember current stimuli with customary repetition
Disorientation
Delirium
Disturbed consciousness with motor restlessness
Transient hallucinations
Disorientation and sometimes delusion
Obtundation
Decreased alertness with psychomotor retardation
Stupor
Not unconscious but exhibits little or no spontaneous activity
Coma
Unarousable and unresponsive to external stimuli or internal needs
Determined by Glasgow Coma Scale
Decorticate
Upper arms held tightly to sides with elbows, wrists, and fingers flexed
Legs extended & internally rotated with feet plantar flexed
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
Causes of decorticate posture
Destructive lesion of the corticospinal tracts within or very near cerebral hemisphere
Causes of decerebrate posture
Lesion in diencephalon, midbrain or pons
Also may be caused by severe metabolic disorders such as hypoxia or hypoglycemia
Flaccidity
No motor response exhibited
Purposeful movement
Localizes to pain stimulus -> unconsciously attempts to remove painful stimulus
Complete flexion
Withdraws or flexes extremity indiscriminately in response to painful stimulus
Focal motor responses
Grasp reflex
Sucking reflex
Babinski reflex
Pupils are unequal or react sluggishly
Compression
Pinpoint or midpoint fixed pupils
Compression of brain stem
Dilated, fixed pupils
Compression of CN III
Unilateral, fixed pupils
Compression of one CN III
Oculomotor responses
Response means intakes brain stem
No response > 48 hours means brain death
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
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
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
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
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
Cluster Breathing
Breathing pattern
Clusters of breaths alternating with irregular periods of apnea Common
Indicates damage to lower pons or high medulla
Ataxic breathing
Chaotic respiratory effort
Indicates damage to the medullary respiratory control center
Hypo or hyperthermia
Hypothalamic or putuitary injuries or with head trauma
Cushing’s Triad
Increased SBP and decreased DBP (increased PP) and decreased HR
Occurs with increased pressure on lower brain stem before herniation
Glasgow Coma Scale
Based on Eye Opening (E), Motor Response (M) and verbal Response (V)
Score lower than 8 need to intibate
GCS Eye Opening
Spontaneous — 4
To call — 3
To pain — 2
None — 1
GCS Motor Response
Obeys commands — 6
Localizes pain stimulus — 5
Normal flexion (withdraw) — 4
Abnormal flexion (decorticate) — 3
Extension (decerebrate) — 2
None (flaccid) — 1
GCS Verbal Response
Oriented — 5
Confused conversation — 4
Inappropriate words — 3
Incomprehensible sounds — 2
None — 1
Arterial blood flow in cerebral circulation
2 internal carotids
2 vertebral arteries > basilar artery
All form the circle of Willis
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
Cerebral arteries
Anterior cerebral artery
Middle cerebral artery
Posterior cerebral artery
Anterior choroid artery
Basilar artery
Regulation of cerebral blood flow
Through auto regulatory or local mechanisms that respond to metabolic needs
Regulation of deep cerebral blood flow
Auto-regulatory
Regulation of superficial cerebral blood flow
Sympathetic
Responsible for vasospasm seen in cerebral aneurysm rupture
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
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
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
Ischemic stroke
Most common type
Caused by an interruption of blow flow in a cerebral vessel of thrombotic or embolism origin
Thrombotic origin
Most common cause of ischemic stroke
At the site
Plaque build up
Increased calcium deposit
Embolic origin
Clot traveled there
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
AV malformation
Arteries and veins clustered and tangled so prone to bleeding and clots
Stroke aftermath
If you a stroke you are much more likely to have another stroke
Most important modifiable risk factor for stroke
Hypertension
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
Bifurcation
Where the blood vessels split into two
Most common spot for am embolism to land
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
Causes of TIA
Atherosclerotic disease and emboli
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
TIA diagnosis
CT scan
Cerebral vascular arterial imagining
Cardiac imaging
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
Carotid endaterectomy
Surgical procedure if you have 1+ TIAs or mild strokes in the past 6 months and carotid stenosis
Risk: cutting the vessel
Extracranial - intracranial bypass
Surgical procedure that redirects blood flow from an artery in the scalp through the cranium to cerebral arteries
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
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
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
Causes of Lacunar Infarcts
Embolism
Hypertension
Small vessel occlusive disease
Hematologist abnormalities
Small intracerebral hemorrhages
Vasospasm
Cardiogenic embolic stroke
Usually affects smaller cerebral vessels, often at bifurcations
Sudden onset with immediate maximum deficit
Most common site of cardiogenic embolic stroke
Middle cerebral artery distribution * offers the path of least resistance
Predisposing conditions for cardiogenic embolic stroke
Rheumatic heart disease
Arterial fibrillation
Recent MI
Ventricular aneurysm
Bacterial endocarditis
Heart Disease and cardiogenic embolic stroke
Tx of HD decreases the incidence of embolic strokes
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
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
Hemorrhagic Stroke
Hemorrhagic stoke 2
Rupture of a blood vessel and bleeding into the brain
- edema
- compression of brain contents
- spasm of adjacent blood vessels
Most common predisposing factor of hemorrhagic stroke
Hypertension
Causes of hemorrhagic stroke
Aneurysm
Spontaneous intracerebral hemorrhages
AV malformations
Other: trauma, erosion of the vessels by tumors, coagulopathies, vasculitis, drugs
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
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
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
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
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
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
Brain area involved in posterior cerebral artery occlusion
Occipital lobe
Anterior and medial portion of temporal lobe
Thalamus involvement
Cerebral peduncle involvement
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)
S/S of occlusion of posterior cerebral artery affect thalamus involvement
Loss of all sensory modalities
Spontaneous pain
Intentional tremor
Mild hemiparesis
Aphasia
S/S of occlusion of posterior cerebral artery affecting cerebral peduncle involvement
Oculomotor nerve palsy with contralateral hemiplegia
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)
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)
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
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
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
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
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)
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
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
Long term disabilities of strokes -aphasia
Encompasses varying degrees of inability to comprehend, integrate and express language
Most common cause of aphasia
Middle cerebral artery of dominant hemisphere
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
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
Dysarthria
Imperfect articulation of speech sounds or changes in voice pitch or quality
Caused by disturbed motor control
Ataxia
Defective muscular coordination
Agnosia
Inability to recognize an object - may be tactile, visual, or auditory
Involves structural damage to association centers of parietal, temporal and occipital lobes
Alexia
Word blindness
Anomia
Difficulty recognizing or naming objects or colors
Conduction aphasia
Inappropriate word use despite good comprehension
Results from destruction of fibers connecting Wernicke’s and Broca’a areas
Neologisms
Invented words
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)
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”
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”
