Download Week 6/7/8: Neurological Disorders Week 6: General Effects of

Week 6/7/8: Neurological Disorders
Week 6: General Effects of Neurological Dysfunction
General Damage
Local Effects: damage to a specific area in the brain will influence a specific body part
 Supratentorial Lesion: above tentorium cerebella. Leads to specific dysfunction in discrete area
 Infratentorial Lesion: below tentorium cerebella. Affects many motor and sensory fibers.
Widespread/generalized impairment.
Left and Right Hemisphere Damage
 Left Hemisphere: Cognitive functions and communication
 Right Hemisphere: personality, relationships and spatial orientation
Consciousness
Decreased Consciousness: Loss of attention and awareness
 Related Structures: cerebral cortex and RAS in brainstem
 Causes: extensive supratentorial or minor infratentorial lesions, pressure on brainstem and RAS,
acidosis and hypoglycemia
States of Consciousness
 Coma: state of unconsciousness and lack of wakefulness. No response to painful or verbal
stimuli. Body is flaccid although reflex present.
 Deep Coma: same as coma but the patient has no reflexes.
 Vegetative State: state of unconsciousness and wakefulness. Respiratory, cardiovascular and
autonomic functions still functional.
 Locked In Syndrome: Conscious but is paralyzed because of brain damage.
 Brain Death: Significant damage to brain cells can cause loss of activity in the brain. The
diagnosis of brain death depends on brain function, brainstem reflex and spontaneous
respirations when ventilator assistance is withdrawn.
Motor Dysfunction
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Related Structures: Upper motor neurons in the cortex, corticospinal tracts, lower motor
neurons in the anterior horns
Contralateral Weakness: Damage to the upper motor neurons in the cortex interferes with
voluntary actions. Effects are contralateral as the corticospinal tracts crossover in the medulla
o Hyperreflexia: Loss of muscle tone inhibition from the brain causes an↑ in muscle tone
and reflex because spinal cord continues to conduct impulses
 Contracture develops
Ipsilateral Weakness: Damage to lower motor neurons in the anterior horns of the spinal cord
Involuntary Posturing: An abnormal posture that results when severe brain trauma occurs
o Decorticate: Severe damage to cerebral hemisphere. Upper limbs are flexed and wrists
are turned inward. Posture a mummy takes.
o Decerebrate: Brainstem lesions and CNS depression. Limbs are extended while head and
back arched. All parts of the body extend.
Sensory Deficits
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Loss of touch, pain, temperature and position: damage to somatosensory cortex
Loss of the other senses: damage to cranial nerves or assigned area of the brain
Hemianopia
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One Eye Blindness: Optic nerve damage
Both Eyes Blind: Optic chiasm (crossover)damage
One Sided Vision: Occipital lobe/optic tract damage on contralateral hemisphere to vision
Language Disorders
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Expressive (Motor) Aphasia: Broca’s Area damage. Impaired oral or writing ability
Receptive (Sensory) Aphasia: Wernicke’s Area damage. Impaired information processing
Global Aphasia: Combination of expressive and receptive aphasia
Dysarthria: Motor Dysfunction. Damage to cranial nerve or muscle impairment. Impaired oral.
Agraphia: impaired writing.
Alexia: impaired reading.
Agnosia: impaired recognition or association
Seizures
Seizures: spontaneous or excessive neuronal discharge
Pathophysiology: Neurons become hyperexcitable and have a lower threshold for stimulation. Any
sensory stimulus can easily activate the affected neurons and stimulate the neighboring neurons.
Causes:
 Rapid Stimuli (ie. flashing lights)
 Infection: Causes inflammation
 Vascular Disease: Hypoxia, ischemica, stroke, shock, dysrhythmia
 Trauma: Bleeding and direct damage
 Neoplastic Disorders: Tumor
 Metabolic Disorders: Fluid electrolyte imbalance
General Signs and Symptoms
 Decreased Self Esteem: Affects school, work and social activities
 Convulsions: Involuntary spasms of skeletal muscle
Types of Seizures:
 Generalized: Multiple origins
o Absence: Appears to be daydreaming/ staring at nothing
 Brief loss of awareness and transient facial movements.
o Tonic-Clonic: Person has convulsions. May arise from simple seizures.
 Aura: Peculiar visual or auditory sensation right before loss of consciousness
 Tonic: Strong muscle contraction (Rigidness)
 Respiration Stops: abdominal and thoracic muscle contract to release a cry.
 Leads to acidosis and hypoxia
 Clonic: Alternation of contraction and relaxation (Jerky)
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Partial: Single origin. Caused by specific stimuli.
o Simple Partial: Caused by repetitive stimuli. May lead to tonic-clonic.
 Jacksonian Seizure: Clonic contractions start in specific area and spreads
o Complex Partial: Person is unresponsive and starts repetitive behaviors
 Caused by temporal lobe, frontal lobe and limbic system damage
 Aura may be present
 May feel déjà vu
Seizure Drugs
 Benzodiazepine: Strengthen GABA activity on Chlorine-ion channels
 Barbiturate: Strengthen GABA activity on Chlorine-ion channels
 Hydantoins and Phenytoin-like drugs: Inhibit Sodium Pump action.
Increased Intercranial Pressure
Pathophysiology: Increase in ICP causes less blood to enter and brain tissue compression leading to
brain cell death at a localized area. This eventually becomes widespread as pressure spreads out.
Etiology
 Increase in fluid or fluid pressure: CSF, Blood, Edema
 Abnormal growth or protrusion of structures in the brain: Trauma, Tumors
Signs and Symptoms
 Early Signs
o Severe headache: stretching of dura and walls of large blood vessels
o Projectile Vomiting: pressure stimulating emetic centre of medulla
o Papilledema: increased ICP and swelling of optic disc (where optic nerve enters)
 Vital Signs
o Cushing’s Reflex: A big conflict of interests created by ICP that fluctuates heart rate and
blood flow. This will cause ICP to continue to rise. BP and pulse pressure increases.
 Cerebral ischemia develops  necrosis
 Vasometer increases blood supply to the brain to counter necrosis
 Vasoconstriction occurs to increase blood pressure to force more blood into
brain (counteract high pressure of ICP)
 Baroreceptors respond to increased BP by slowing heart rate (bradycardia)
 Chemoreceptors respond to low CO2 levels by reducing respiratory rate
 Improved cerebral circulation temporarily relieves ischemia but also increases
ICP again so ischemia will come back and cycle is repeated
o Damage: Severe ischemia and neuronal death cause damage to brain function
 Prevent circulatory and respiratory control
 Blood pressure drop
 Cheyne-Stokes Respiration: alternating apnea (periods of no respiration) and
periods of fluctuating respiration rates (increase or decrease)
 Visual Signs
o Pressure on Cranial Nerve III (Oculomotor)
 Unresponsive and Dilated Pupils (Blown)
 Ptosis (Droopy Eyelid)
Week 8: Acute Neurological Disorders
Transient Ischemic Attack
Pathophysiology: Ischemia from Partial Blockage of Blood Vessels causes temporary loss of function
Signs and Symptoms
 Muscle weakness in extremity
 Visual disturbances
 Numbness and Paresthesia in face
 Transient Aphasia (Confusion)
Cerebrovascular Accident (Stroke)
Pathophysiology: Infarction of brain. Results in permanent loss of neurons (cysts)
 Categories:
o Atheroma: Atherosclerosis develops slowly clogging the artery. Most likely results in TIA
o Embolus obstruction: Embolus clogs the cerebral artery. Most likely a sudden onset.
o Intracerebral hemorrhage: Rupture in cerebral artery from hypertension.
 Causes ICP
 Most destructive. Affects large portions of the brain.
 Blood in interstitial area causes vasospasm, electrolyte imbalance, acidosis,
cellular edema
Etiology:
Risk Factors:
o Diabetes
o Atherosclerosis
o Hypertension
o Heart Disease
o Systemic Lupus Erythematosus
o Increasing Age
o Elevated Cholesterol levels
o Oral Contraceptives
o Hyperlipidemia
o Cigarette Smoking
Symptoms: Dependant on area of blockage.
o Large Artery  Widespread
 Coma
 Loss of consciousness
 Death
o Anterior cerebral artery  frontal lobe
 Weakness or paralysis, sensory loss in leg, confusion, loss of problem solving
skills, personality changes
o Middle cerebral artery  cerebral hemisphere
 Contralateral paralysis and sensory loss, aphasia if dominant hemisphere is
affected, spatial relationships when right side is damaged
o Cyst Formation: Necrotized Brain Tissue
Transient Ischemic Attack vs. Cerebrovascular Accident
TIA (Short Term)
Medical Implications
Warning Sign
Consciousness
Intact
Symptom Duration
1 hour – 2 hours
Recovery
Within 24 hours
CVA (Long Term)
Damage
Lost
Depends on medical care
Depends on medical care
Head Injury
Head Injury: Blow to the Head causing
 Concussion: Excessive movement of the brain  impact. Temporary interference of function.
Loss of consciousness. Mild blow.
 Contusion: Bruising of brain. Involves rupturing of blood vessels and edema. Various degrees.
 Closed: skull not fractured
 Open: skull fractured or penetration via projectile
Pathophysiology of Head Injuries
 Primary: Direct Damage
o Laceration
o Shearing Injury
o Compression
o Necrosis and Loss of Function
 Secondary: Additional Effects resulting from Primary Damage (ie. Bleeding)
o Hematoma: Collection of Blood in Tissue
 Types:
 Epidural Hematoma (Dura – Skull): Meningeal Artery ruptures.
 Subdural Hematoma (Dura – Arachnoid): Tear in Vein. Slow build up
o Acute: within 24 hours
o Subacute: ICP within a week
o Chronic: May occur in elderly. More brain atrophy = more space
 Subarachnoid Hemorrhage: Blood mixes with CSF so it always circulates
 Intracerebral Hematoma: Contusions or Shearing Injury
 Hemolysis: Draws more water in to exacerbate ICP
 Vasoconstriction: Furthers Ischemia
o Herniation: Displacement of Brain Tissue via abnormal mass (ie. Tumor, blood clot, etc)
Signs and Symptoms
 Seizure: Blood irritating mucosa
 Cranial Nerve Impairment: Basilar Fracture
 Otorrhea/Rhinorrhea (CSF leakage): Fracture and tearing of meninges
 Otorrhagia (Blood leakage): Fracture site with torn vessels and meninges
 Fever: Infection
 Stress Ulcers: ↑ Gastric secretion
 Immobility: Loss of consciousness
Diagnostics
 Computed Tomographic (CT) Scans: Extent of Brain Injury
 Simplified Head Injury Assessment: Awakening the patient periodically to check consciousness,
pupil reaction, signs of sickness and change in behavior or movement.
Treatment
 Glucocorticoids: For edema (leading to ICP)
 Antibiotics: For infection
 Surgery: Reduce ICP or remove foreign material
 Blood/ Oxygen Products: Protect brain tissue from necrosis
Week 9: Chronic Neurological Disorders
Multiple Sclerosis
Multiple Sclerosis: Demyelination disorder leading to loss of nerve function.
Pathophysiology
 Demyelination: A myelin sheath is required to speed up nerve impulses. Nerve impulses from
cells which lack myelin are either slow (delayed response) or do not conduct (loss of function)
o Plaques: Areas of inflammation and demyelination (appear whitish)
 Usually in the lateral ventricles, brainstem and optic nerves
 Intellectual Functions: not usually affected
 Early Stages
o Lesions occur as inflammatory response with loss of myelin in white matter
o Neural function may return to normal after the initial inflammation but repeated
incidents cause neural degeneration to be permanent
Etiology
 Age: 20-40; Peak: 30
 Gender: Twice as common in women
 Autoimmune disorder: Immune system attacks myelin.
 Genetic: European
 Environmental Components: Temperate zones/climates
Signs and Symptoms
 Local Manifestations: Symptoms depend on location of multiple sclerosis
o Common/General: Blurred Vision
o Corticospinal: Weakness in legs
o Cranial Nerves: Diplopia (Double Vision), Dysarthria (Poor Articulation/ Expression),
Scotoma (Spot in vision)
o Sensory Nerves: Paresthesia (Numbness, Burning, Tingling)
 Later Stages
o Weakness and paralysis extend to upper limbs, loss of coordination, bladder, bowel and
sexual dysfunction
o Chronic fatigue
o Depression or euphoria
Diagnostics: use MRIs to find lesions
Treatment: No Cure. Medication is used to slow down the disorder.
 Glucocorticoid: control acute signs in exacerbations
 Interferon beta-1b: reduce frequency and severity of exacerbations
 Reducing Physical Stresses (Fatigue, stress, injury, infection): ↓ Exacerbations
Parkinson’s Disease (Paralysis Agitans)
Parkinson’s Disease: degenerative disorder affecting motor functions.
Pathophysiology
 Degeneration of Basal Nuclei: ↓ dopamine secretion causes an imbalance between excitation
and inhibition as dopamine is inhibitory. This leads to excessive neural and muscular stimulation
 Reduced Cortical Neurons: Characteristic of Dementia
Etiology
 Primary
o Age: usually 60+
o Genetics
o Viral and Toxic Damage
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Secondary
o Encephalitis
o Trauma
o Vascular Disease
o Phenothiazine
Signs and Symptoms
 Overwork of Muscles:
o Fatigue
o Muscle Weakness
o Muscle Aching
 Involuntary Contraction
o Tremor
o Spontaneous Change in Facial Expression
 Increase in Stiffness
o Muscle rigidity and inflexibility
o Bradykinesia (slow movement) and lack of involuntary movement
o Difficulty initiating voluntary movement and propulsive gait (↑ falling risk)
o Chewing/swallowing slows (increases eating time and drooling)
o Mask-like face and dysarthria (hard time articulating words)
o Stooped posture
 Dementia
Treatment: No cure
 Dopamine Replacement Therapy: reduce motor impairment.
o Levodopa (l-dopa): a precursor to dopamine is administered because dopamine itself
does not cross the blood brain barrier
o Selegiline (Eldepryl): blocks breakdown of levodopa
 Anticholinergic drugs: reduce effects of acetylcholine. Acetylcholine involved in muscle
contraction and tone
 Physical therapy: maintain general mobility
 Speech and language Pathologist: maintain speech function
Parkinson’s Drugs
Dopaminergic Drugs: Restore dopamine function or stimulate dopamine receptors. Doses lowered
gradually on discontinuation.
Anti-cholinergic Drugs: Lower acetylcholine levels.
Alzheimer’s Disease
Alzheimer’s Disease: Deterioration of cognitive function from plaque and neurofibrillary formation.
Pathophysiology
 Cortical atrophy: dilated ventricles (protrusion) and widening of the sulci (valley)
 Neurofibrillary tangles: Microtubule breakdown. Transportation mechanisms impaired.
 Senile plaques: Disrupts neural conduction. Made from beta-amyloid precursor proteins.
o Plaques don’t mean impairment. Depends on size, amount and specific area
 Aceytlcholine Deficiency: Acetylcholine is important in nerve impulse conduction. If a deficiency
occurs, neural impulses may be slowed down or stopped.
Etiology
 Unknown cause
 Gender: More females than males
 Genetic: At least four defective genes are associated with Alzheimer’s
o High incidence in those with Down Syndrome (Trisomy 21)
 Possible Factors: exposure to metals and viruses
Signs and Symptoms
 Insidious (gradual, subtle, harmful). Progresses over 10 to 20 years
Cognitive
Memory
Ability to learn
Ability to concentrate
Intermediate Language skills
Math skills
Judgment
Problem solving
Late
Loss of recognition
Lack of awareness
Loss of interest
Early
Emotional
Irritable
Hostile
Mood swings
Apathy
Indifference
Confusion
Motor/ Routines
Meal preparation
Dressing
Personal hygiene
Wandering
Motor function affected by
degeneration
Diagnostics: No diagnostic tests. Diagnosed based on process of elimination
Treatment: No Cure. Treated based on symptoms. Many drugs not administered because they cause
mental confusion.
 Anticholinesterase: led to temporary improvement from improved cholinergic transmission.
 Daily Routines and Exercise Program: Moderate stimulation to prolong independence.
Alzheimer’s Drugs
Acetylcholinesterase inhibitors: Increase acetylcholine levels by inhibiting its destruction. Doses
lowered gradually on discontinuation.
References
Adams, M., Holland, L. N., & Urban, C. Q. (2011). Pharmacology for nurses: a pathophysiologic approach
(3rd ed., pp. 166, 170-173, 157-159, 263-266). Upper Saddle River, N.J.: Pearson Education.
Gould, B. E., & Buttle, G. (2006). Study guide for pathophysiology for the health professions (3rd ed., pp
536-543, 546-549, 555-560, 577-587). Philadelphia: Saunders/Elsevier.
" Vegetative State: Coma and Impaired Consciousness." THE MERCK MANUALS. N.p., n.d. Web. 28 Mar.
2012.
<http://www.merckmanuals.com/professional/neurologic_disorders/coma_and_impaired_consciousne
ss/vegetative_state.html>.