10 (part 1) nervous system Flashcards
CVA
Most common vascular disorder, third leasing cause of death
Risks for CVA
Same risks as CAD
CVAs 3 pathos
Ischemic thrombus and embolus, hemorrhagic
Ischemic thrombus
Thrombi form in intracranial arteries, gradual onset, possibly TIAs first, minimal ICP
TIAs
Comparative to angina
Ischemia from partial occlusion (not infarction)
All deficits resolve within 24 hours with no residual dysfunction, USUALLY subside after 1-2 hours
How many thrombosis strokes are preceded by TIA
35%
Ischemic embolus
From outside brain, usually obstructs at a bifurcation or point of narrowing
Sudden onset, minimal ICP, localized effects
Hemorrhagic Stroke
Caused by HTN, aneurysms, bleeding disorders, AV malform
Compresses/displaces brain tissue, with seepage into ventricles, sudden onset (often with activity) ICP present, widespread effects
Patho of CVA
Neurons around ischemia area undergo plasma membrane changes resulting in cellular edema resulting in further compression of capillaries, cerebral edema reaches max in 72 hours and takes 2 weeks to subside
Carotid (anterior) CVA
Unilateral paralysis
Numbness
Visual disturbances
Monocular blindness
Vertebrobasilar (posterior) CVA
Vertigo, visual disturbances, diploplia, paralysis, numbness, dysarthia, ataxia
General S&S of CVA
Altered LOC
Walking difficulty
Weakness/numbness on one side of body or in face, arm, grips, legs
Intense headache
Difficulty speaking, comprehending, and/or seeing
ACLS Cincinnati prehospital findings
1 of the 3 have 72% chance of ischemic stroke
All 3 85% chance of acute stroke
LAMS
Face 1
Grip 1 or 2
Arm strength 1 or 2
Causes of cerebral aneurysms
ARteriosclerosis
Congenital abnormality
Embolus
Trauma
Cerebral aneurysms
Often at bifurctions in or near circle of willis
Vertebrobasilar arteries
Within carotid system
Often a change in hemodynamics leads to rupture
Saccular (berry) aneurysms
Probs due to congenital abnormalities in media of arterial wall, gradually grows over time
Lateral and fusiform aneurysms
Diffuse arteriosclerotic changes, most in basilar arteries or terminal portions of internal carotids
Space-occupying lesions, can be due to trauma, rupture causes subarachnoid, intracerebral or combined hemorrhage
S&S of cerebral aneurysm
Severe headache Vomiting CNS depression Meningeal irritation ICP CN deficits Stroke-like manifestations
Warning signs of impending aneurysm rupture
Headache, transient unilateral weakness/numbness/speech
AV malmformation
Cause of both hemorrhagic and subarachnoid
Congenital that leads to a tangle of thin walled arteries being directly attached to veins
Global ischemia
Widespread atherosclerotic narrowing, multiple foci of ishemic necrosis
Over time result in progressive mental deterioration
Bacterial Meningitis infects
Primarily pia mater and arachnoid + fluid in subarachnoid space
Involves the ventricles
Causes of bacterial meningitis
Meningococcus, pneumococcus, haemophilus influenza
Predisposing factor must be present before bacteria can become blood-borne (prior URT infection)
Method of entering CNS is unclear
Patho of bacterial meningitis
Bacteria irritate and cause vascular changes (congestion and increased perm) so neutrophils migrat to sub arach space, inflamm response mediated in meninges, CSF, and ventricles
Purulent exudate is formed and increases rapidly (especially around base of brain and extends to cranial and spinal nerves)
Clinical manifestations of bacterial meningitis
Severe general throbbing headache
Photophobia, C.N damage, diplopia, tinnitus
Neck stiffness, pain and nuchal rigidity (spinal nerve irritation)
Projectile vomiting when vomiting center is irritated
Fever, confusion, decreased responsiveness
Rash of bac meng
Meningococcus septicaemia causes non blanching rash
Viral meningitis
Inflamm limited to meninges
Caused by mumps, herpes simplex, adenovirus
Often undiagnosed
Characterized by a lymphocytic exudate in sub arachnoid space
Neurosyphilis
Stage 3 of syphilis, can present as chronic meningitis
Meninges infiltrated with lymphocytes and plasma cells, loss of neurons correlates with motor and mental changes
Encephalitis
Acute febrile illness of various origins within nervous system involvement
Virus - herpes, west nile
Bacterial - lyme
Parasite - toxoplasmosis (immune suppressed)
Can be a complication of systemic viral disease like rabies mono or follow an MMR vaccine
Patho of encephalitis
Virus causes widespread nerve degeneration
Edema and necrotic areas develop with/without hemorhhage
ICP develops and may progress to herniation
Clinical manifestations of encephalitis
Fever, delirium, confusion to unconsciousness, ceaser, paresis, paralysis, ICP, involuntary movements
Myelitis
Diffuse viral infection of spinal cord
Cerebral Abscess
Localized suppurative infection, consists of cavity filled with pus and a capsule composed of glial cells and fibroblasts
Gillian-Barre Syndrome AKA
postinfectious polyneuritis
Acute idiopathic polyneuropathy
Acute infections polyradiculoneuritis
Etiology of Gillian-Barre
Precise cause is unknown, autoimmune response precipitated by viral infection or immunization
Patho of gillian barre
Periph nerv inflammation
Accumulation in periph nerv of lymphocytes
Demyelination
Axon destruction
Mainly efferent fiber effected
Usually starts low ext and goes up, spontaenous recovery which goes top down
Clinical manifestations of Gillian Barre
Progressive muscle weakness and areflexia in low ext, ascending flaccid paralysis
Paresthesia or pain and general muscle aching
Speech/vision/resp effected
Can be over a few hours or over several days
Autonomic nervous impairment from gillian barre
Common
Cardiac arrhythmias
Labile BP (fast fluctuations of normal to high)
Loss of sweating capability
Poliomyelitis
Highly contagious polio virus
Reproduces in lymphoid tissue (oropharynx and digestive tract)
enters CNS, attacks motor nerves of spinal cord and medulla
Clinical manifestations of polio
Flu like symptoms
Fever, headache, vomiting, stiff neck, headache, flaccid paralysis
Reye’s syndrome
Etiology not fully determined, but occurs with viral infection (infleunza) treated with ASA
Tylenol OK
Pathology occurs within brain and liver
Reye’s pathology
Noninflamm edema leading to ICP
Liver enlargement, fatty changes and progression to failure (without jaundice)
Livere enzymes elevated and altered metabolism lead to encephalopathy
Reye’s syndrome S&S
Manifestation vary in severity
Lethargy, headache, vomiting, diorientation, hyperreflexia, hypervent, ceasers, stupor, coma
MS
Progressive CNS demyelination, not involving PNS
Degen of previously normal myelin with relative preservation of axons
20-40 years age
2:1 male
Patho of MS
Believed to be autoimmune, origins complex with genetic and environmental component
Related to dairy intake, climate (sun/temp) epstein-barr virus
Theories on patho of MS
T-Cell activity
Viral infection creates sensitized T cells to antigen on myelin
B lymphocytes trapped in CNS and colonize forming plasma cells which secrete IgG to combat antigens
More MS patho
Demyelinating lesions (plaques) form, usually involve white matter, scattered patterns causing variable symptoms
Eventually undergo glial scarring with degen of axons (after 20+ years)
Axons will transmit slower, progressive loss to permanent disability
Clinical manifestations of MS
Initial syndroms followed by remissions and established perm syndromes
Most commonly corticospinal, stiffness, slowness, weakness
More clinical manifestations of MS
Spastic paraparesis, atxia, bladder dysfunction, paresthesia, CN III - XII dysfunction, eye problems, depression
Thiamine (B1) deficiency
B1 essential for neurons energy
Also for acetylcholine
Wernicke’s is a
B1 deficinecy (wernicke’s encephalopathy) goes with korsakoffs pyschocosis
Wernicke’s
Acute but reversible encephalopathy,
Ataxia, eye muscle weakness, mental derangement
Korsakoffs (psychosis) in 80% of wernicke’s pts, memory disorder
Wernicke-korsakoff sydnrome (aka cerebral beriberi)
Triad of ocular function, gait, mental function
B12 (isbalamin) has a role in
DNA synthesis
RBC maturation
facilitation of folate metabolism
Erythrocytes
B12 deficiency
Uncoordianted movement and sensorimotor peripheral neuropathy with signs of spinal cord disease
Demention
Depression
Pernicious anemia
Pellagra
Diarrhea, dermatitis, dementia from niacin (b3) deficiency
Acetaldehyde (ETOH) causes
HTN Pancreatitis Skeletal muscle regression Liver damage Immune disorders Cerebral atrophy Neuronal cell development in fetus is affected
ETOH absuers prone to
subdural hematomas
Alzheimer characterized by
Atrophy of cortical parts of frontal and temporal parts of brain
Patho alzheimer
Protein in cerebral neurons become distorted and twisted forming a neurofibrillary tangle
Groups of nerve cells degenerate and coalesce around amyloid core
Amyloid deposited in cerebral arteries
Possible causes of alzheimers
Loss of neurotransmitter stimulation by choline acetyltrasferase
Linked to genetic chromosomal changes
Onset usually after 65
Clinical manifestations of alzheimers
Forgetfulness, emotional, disoreintation, confusion, decreased concentration abstraction and problem solving
Irritability, agitation, restlessness, anxiety, mood swings
Parkinson
Disorder of basal ganglia involving dopaminergic nigrostriate, onset after 40
Changes in extrapyramidal motor system of mid brain
Dopamine (inhibitory) is decreased in striatum
Clinical manifestations of parkinsons
Tremors, rigidity, bradykinesia (slowing) postural instability, tremors/twitching (most prominent in hands), involuntary flexion of head and neck
Worsened by emotional stress
Short shuffling accelerated steps, 10% have progressive dementia
Parkinsons face
Wide-eyed unblinking, staring expression, immobile axial features, drooling from side of mouth
Huntington’s Disease (chorea)
Rare, genetic, degeneration of basal ganglia and cerebral cortex
Onset 40-50
From depletion of GABA which acts inhibitory on dopaminergic neurons
Patho of huntington’s
Excess of dopaminergic activity in basal ganglial feedback circuit and cerebral cortex (due to lack of GABA)
Manifested by hypotonia, hyperkinesia, involuntary, fragmented movements
Clinical manifestations of huntington’s
Abnormal movements (chorea) progressive dysfunction in intellectual processes (dementia) delusions, depression, impaired memory
Amyotrophic Lateral Sclerosis (Lou Gehrigs)
Sporadic motor neuron disease
Occurs between 30-50 years old
Amyotrophic definition
“amyotrophic” -progressive wasting (refers to lower motor neuron involvement)
Lateral Sclerosis definition
“lateral sclerosis” - scarring of corticospinal tract in lateral spinal column (refers to upper motor neurons)
ALS patho
Upper and lower motor neuron degeneration without inflammation
Leads to generalized muscle loss and death (from resp function loss)
Clinical manifestations of ALS
Weakness (any/all muscles)
Paresis (single muscle group, progresses)
Not extraocular or heart muscles
Progression to paralysis, no remission
No mental, sensory or autonomic symptoms present
3-5 years average life
Prone to resp problems
Types of headaches
Associated with congested sinuses, nasal congestion
Temporal headache from TMJ disorder
Increased ICP - trauma with edema, TUMAH, meningitis, toxins (ETOH)
Migraine
Tension
Sphenopalatine ganglioneuralgia
Migraine
Benign, recurring headache often provoked by trigger
Often prodromal period
Migraine triggers
Stress, hunger, weather changes, foods, sunlight and often accompanied by neurologic dysfunction
Prodromal period of migrains
Aura, hallucinations, nausea
Pain of migraine
Throbbing, severe, ca be incapacitating
Begins in temporal regions and spreads to entire head
Symptoms of migraine
Pain, visual disturbances, dizziness, nausea, abdo discomfort, fatigue
Last for 24 hours with long recovery periods
Patho of migraines
May be due to abnormalities in cerebral blood (constriction then dilation)
Have have a reduction in brain and electrical activity, or increase release of serotonin
Tension headache
Most common Onset in teens Bilat, mild to moderate steady pain Persist for days or weeks Possibly vomiting
Tension headache etiologies
Hypersensitivity of pain fibers (trigeminal nerve)
Spasms of neck muscles which pulls down scalp
Two types of neoplastic disorders (headaches)
Primary - origination from cerebral tissue itself. Rarely metastasize, but may have multiples. Gliomas most common category (from neurolgia or glial cells)
Secondary- metastasis from either the breast or lungs
Histology neoplastic disorders
Astrocytes, oligodendrolgia, pineal, benign vs malignant
Brain stem and cerebellar tumors in young children
Researching focusing on prenatal parental exposure to carcinogens
Tumors in mid adult life
Cerebral hemisphere most common
Predisposing factors not established
Some risk factors for CNS neoplasms
Genetics, ionizing radiation (10x risk, glial tumors 3-7x)
Cell phones, high voltage wires, hair dyes, trauma, dietary n-nitrosourea
*all have conflicting evidence
Malignant tumors
Have no definitive margins, invasive invaginations
Neoplasms patho
Malignant primary tumors have no definitive margins, surrounding tissue becomes inflamed, contributes to pressure
Obstruction of CSF production and flow at >5 ICP
Clinical manifestations of neoplasms
Depend on location
Small tumors of stem or pituitary immediately alter function
Large tumors of cortex can grow without symptoms
Eventually, headache from minor to severe and more frequent
Vomiting
Lethargy
Irritability
Personality/behaviour changes
Seizure - focal to generalized
Brainstem or cerebral tumors can affect cranial nerves
