Disorders of Brain Function Flashcards
Differentiate cerebral hypoxia from cerebral ischemia and focal from global ischemia.
- Focal Cerebral Ischemia = short term
- Typical causes: thrombus/embolism
- “zone of penumbra” without infarction - Global Ischemia = Loss of Consciousness
- Release of “excitatory” amino acid neurotransmitters
- Disruption of calcium balance
- Formation of free radicals (instability with free electron floating around)
- Mitochondrial injury
- ATP malfunction = “power failure” = edema
If not restored quickly, permanent damage!
Characterize the role of excitatory amino acids as a common pathway for neurologic disorders.
- Neuron injury results in release and activation of mediators that overstimulate cell receptors
- Amino acids (e.g. glutamate), catecholamine’s, free radicals etc. - Glutamate attaches and opens calcium channels leading to “calcium cascade” into cells
- Protein breakdown
- Free radical formation
- DNA fragmentation
- Mitochondrial injury
- Cell death
Compare cytotoxic and vasogenic cerebral edema
- Vasogenic
- Leaking of water/proteins into Interstitial space
- Causes: hemorrhage, meningitis, injury, tumors
- White matter more so (not as dense as gray)
- Result: herniation, focal defects, increased intracranial pressure, altered LOC - Cytotoxic
- Increased intracellular fluid
- Causes: water intoxication, impaired K+/Na+ pump
- Result: cell rupture with damage to surrounding tissue, - increased intracellular fluid
State the determinants of increased intracranial pressure and describe the typical symptoms associated with this condition.
Compartment syndrome in the skull
- Intracranial pressure greater than arterial blood pressure
- Arteries collapse; blood flow to brain cut off
Compliance = change in volume change in pressure - Tissue: tumor, edema, bleed
- Blood: vasodilation, obstruction of outflow
- CSF: increased production, decreased absorption, obstruction
Compare the causes, manifestations, and usual treatment of communicating and noncommunicating hydrocephalus
- Increased CSF volume enlarges ventricles and compresses brain tissue
1. Non-communicating/Obstructive - Congenital malformations, tumors, inflammation, hemorrhage = CSF blockage
2. Communicating - Impaired reabsorption of CSF via arachnoid villi d/t infection, scarring, blockage by lyzed rbcs post repair of bleed
- Increased production of CSF (rare)
Manifestations
- Fontanel bulging fetus/newborn
- Signs of increased ICP in all ages
- Optic nerve atrophy/blindness
Differentiate primary and secondary brain injuries due to head trauma.
1. Primary/Direct injuries—due to impact Microscopic damage: diffuse axonal injury Contusions Coup (place of impact) Contrecoup (injury that occurs as a result of brain moving due to impact) 2. Secondary injuries—due to: Ischemia Hemoorage Infection Increased intracranial pressure
Describe the mechanism of brain damage in coup-contrecoup injuries.
- a coup injury occurs under the site of impact with an object
- a contrecoup injury occurs on the side opposite the area that was hit
Describe the symptoms associated with mild, moderate, and severe traumatic head injuries.
- Mild
- Concussion (immediate & possible post-concussion syndrome)
- Limited symptoms to momentary LOC, residual amnesia - Moderate
- Small hemorrhages, edema
- LOC, cognitive/motor deficits, hemiparesis, nerve palsies - Severe
- Shearing, pressure = axon/vessel/tissue damage
- Extensive damage with secondary manifestations- Hemiplegia, signs of elevated ICP, coma
Differentiate among the location, manifestations, and morbidity of epidural, subdural, and intracerebral hematoma.
- Hematoma - Epidural
- Meningeal artery tear
- Rapid bleeding; unconsciousness may be followed by brief lucid period
- Ipsilateral pupil dilation, contralateral hemiparesis d/t uncal herniation
- Treatment prior to LOC has good prognosis - Hematoma- Subdural
- Venous tear between dura & arachnoid
- Slower bleeding
- Acute (within 24 hours)
- Increased ICP, decerebrate posturing, LOC, high mortality rate
- Subacute (2-10 days)
- Periods of improvement prior to rapid deterioration
- Chronic (weeks)
- Slow bleed, decreased LOC, drowsiness, confusion, apathy, h/a - Hematoma- Intracerebral
- Usually frontal or temporal lobes
- Risk: age, alcoholism
- Symptoms dependent on size & location
- Increased ICP
- herniation
Discuss Doll’s eyes response, decorticate and decerebrate posturing, and Cheyne-Stokes breathing as they relate to diffuse brain injury.
- Doll’s eyes response: (vestibulo-ocular reflex)
- Indicates brain stem damage
- Possible tentorial herniation - Decorticate posturing
- Damage to one or both corticospinal tracts involving the “red nucleus” in midbrain - Decerebrate posturing
- Indicated brain stem damage below level of red nucleus
- Upper & lower extremity extension
- Head arched back
- Can be one side or both or just arms - Cheyne-Stokes
Differentiate the pathologies and risk factors of ischemic and hemorrhagic stroke.
- Ischemic Stroke (interruption in blood flow)
- Age, gender, race, familial, HTN, smoking, DM, sickle cell disease, atrial fibrillation, CAD
- Obesity, physical inactivity, alcohol, drug use, - - - hypercoagulability disorders, oral contraceptives, - hormone replacement therapy - Hemorrhagic Stroke (bleed into brain tissue)
- HTN, aneurysms, AV malformations, head injury, blood dyscrasias
Explain the significance of transient ischemic attacks, the ischemic penumbra, and watershed zones of infarction and how these conditions relate to ischemic stroke.
Transient: - Focal cerebral ischemia - “zone of penumbra” without infarction - Reverses prior to ischemia - Similar risk factors and symptoms as stroke but symptoms last < 1 hour with fully recovery Increases risk of stroke
Describe the progression of motor deficits and problems with speech and language that occur as a result of stroke.
- Usually unilateral and focal
- Weakness/numbness (face, arm, leg)
- Vision loss
- Aphasia (language disorder)
- Dysarthria (motor speech disorder)
- Ataxia (muscle coordination disorder)
Cite the most common causes, manifestations, and possible complications of subarachnoid hemorrhage.
- Risk factors of aneurysm
- AV malformations of brain
- Atherosclerosis
- Polycystic kidney
- Coaractation of aorta - Risk factors of rupture
- Age
- Smoking
- HTN
- Alcoholism
- Size of aneurysm
- Conditions that increase ICP - Pre-rupture
Sudden-onset headache with n&v, dizziness
Hemorrhage
- Sudden severe h/a, N&V, nuchal ridigity, photophobia, vision and motor problems, loss of consciousness
Complications post-op
- re-bleeding, vasospasm, hydrocephalus
Describe the alterations in vasculature that occur with arteriovenous malformations.
- Tangle of abnormal arteries and veins linked by fistulas
- Possibly due to lack of capillary formation invitro
- Structurally unstable with high pressure flow from - arteries to veins
- Ischemic symptoms
- Symptoms may not show until > 40 yrs of age
- Hemorrhage usually slower process
- Surgical removal
Compare the pathophysiology and manifestations of acute bacterial and viral meningitis
Acute Bacterial Meningitis:
- Inflammation of pia, arachnoid and subarachnoid space
- Contagious: direct contact (blood/mucous)
- Carriers
- 10% permanent damage (ear, sight, etc.)
- 10% fatal
- Neisseria meningitidis or Streptococcus pneumoniae
- Group B streptococci (neonates)
Acute Bacterial Meningitis Risk Factors
ABM risk Factors:
- Basilar skull fracture
- Otitis media
- Sinusitis/mastoiditis
- Neurosurgery
- Sepsis
- Living in close quarters/aged/infants
Acute Bacterial Meningitis patho:
ABM patho:
- Bacteria replicate & lyze in CSF
- Endotoxins/debris result in inflammatory process
- Neutrophils/albumin etc. allowed into CSF
- Thrombi, scarring, blockage
Compare the pathophysiology and manifestations of acute bacterial and viral meningitis
Acute Bacterial Meningitis:
- Inflammation of pia, arachnoid and subarachnoid space
- Contagious: direct contact (blood/mucous)
- Carriers
- 10% permanent damage (ear, sight, etc.)
- 10% fatal
- Neisseria meningitidis or Streptococcus pneumoniae
- Group B streptococci (neonates)
Viral Meningitis:
Acute lymphocytic
Enteroviruses, Epstein-Barr virus, mumps virus, HSV, West Nile
Similar to bacterial but less severe
CSF has: lymphocytes and small amount of protein only, normal sugar
Self-limiting unless herpes simplex virus type 2 (HSV-2) which requires acyclovir
Describe causes and usual manifestations of encephalitis.
- Parenchymal infection of brain or spinal cord
- Usually viral
- HSV
- West Nile
Manifestations
- Lethargy, disorientation
- Fever, h/a, nuchal ridig
- Seizures, paralysis, delirium, coma
Diagnosis with LP/CSF investigation
Describe the various types of brain tumors based on their origins and progress
- Most often secondary site of metastasis
Primary more common in children (mortality rate 45%)
Risks: genetics, high-dose radiation
Rarely benign, but if so, still dangerous
Pressure
Attachment = difficult to excise
Neurogliomas of astrocytic origin
Medulloblastomas
Acute Bacterial Meningitis manifestations
- h/a, fever, nuchal rigidity
- N&V, photophobia, altered menation
- Petechial rash/palpable purpura (N. meningitis)
- Seizures, cranial nerve palsies, focal cerebral signs
ABM diagnosis and treatment
> Diagnosis
Lumbar puncture (LP): cloudy, purulent
Kernig sign
Brudzinski sign
> Treatment
Antibiotics
Neuroglial tumors
Most common primary tumor
- Graded I to IV
- Astrocytes: protective cells, protect neurons, supply nutrients/oxygen
- Oligodendrocytes: supportive cells in brain, eg. Form myelin
- Ependyomal: line ventricles & spinal cord
Explain the difference between a seizure and epilepsy.
Seizure: - Temporary alterations in cerebral activity - Causes are numerous - Provoked = - Fever (children) - Metabolic condition (adults) - Structural changes - Cellular changes - Unprovoked/idiopathic = epilepsy - Genetic Epilepsy: - Seizure activity that doesn’t cease on own or occurs successively - High mortality rate - Must treat cause
Discuss possible causes of provoked seizure activity
- Fever (children)
- Metabolic condition (adults)
- Structural changes
- Cellular changes
Differentiate between the origin of seizure activity in partial and generalized forms of seizures.
- Partial:
- Simple Partial/Elementary
- One hemisphere only
- No loss of consciousness
- Symptoms dependent on area involved
- Motor may cause “jacksonian march”
- Sensory symptoms may be only sign
- No observable symptoms
- Prodrome/aura is not just a warning!
- ANS involvement (tachycardia, diaphoresis, - hypo/hypertension, pupil changes, etc.) - Generalized:
- Absence (“petit mal”)
- Generalized disturbance of consciousness
- Blank stare, often motionless or automatisms
- Lasts only seconds so can be overlooked
“atypical” type has slow onset/end
Atonic (“drop attacks”)
Sudden loss of muscle tone
Describe the changes in brain tissue that occur with Alzheimer disease.
Neuritic (senile) plaques
Accumulation of amyloid peptide
Degenerative nerve terminals with an amyloid core
Neurofibrillary tangles
Decreased enzyme that synthesizes acetylcholine
Neurotransmitter associated with memory.
Use the three stages of Alzheimer disease to describe its progress.
- Initial: subtle
Loss of memory and denial of same
Mild personality changes: withdrawal/loss of sense of humor - Moderate stage
Loss of higher cortical functions (problem solving)
Depression if aware of changes
Hostility
Sundown syndrome - Late stage
Loss of the ability to respond to environment/family
incontinence
Vascular Dementia
Ischemic or hemorrhagic damage (MI, arrhythymias, DM, PVD, infection, smoking)
Slow psychomotor functioning
Depression is common
Metastatic tumors
Melanomas to frontal & temporal lobes
Breast Ca to cerebellum & basal ganglia
NSC lung Ca to occipital lobe
Frontotemporal Dementia (PICK)
Atrophy of frontal and temporal lobes
Progressive syndrome
Behavioral changes common
Impulsiveness, loss of inhibitions (social behaviour), apathy
Language/understanding issues are less common but do happen
Death d/t infection in 2-10 years
Diagnosis: Neuroimaging
Creutzfeldt Jakob Disease
Rapid, infective protein “prion” Bovine spongiform encephalopathy (BSE) “mad cow disease” Dementia within 6 months of infection Results in degeneration of pyramidal and extrapyramidal systems
Creutzfeldt Jakob Disease manifestations
Personality changes Visual/spatial coordination issues Impaired memory & judgement Extreme dementia Insomnia Ataxia Death in months
Wernicke-Korsakoff Syndrome
Cause is typically thiamine deficiency as a result of chronic alcoholism Manifestations: Weakness of eye muscles Delirium, confusion, hallucinations Memory loss with confabulation polyneuritis
Physical symptoms are somewhat reversible with nutrition, thiamine, but not “psychosis”
Huntington Disease
Cause is hereditary
Emerges in 40-50’s
Cell death in basal ganglia motor control
Manifestations
Chronic progressive chorea (jerky movements)*/dyskinesia (impaired movement)
Psychological changes
Cognitive decline, dementia
Cushing Reflex: Late sign of ICP
- HTN
- Widening pulse pressure
- Reflex bradycardia
Astrocyte tumor: Infiltrating/non-infiltrating
Astrocyte
Infiltrating (middle adult)
Usually cerebral hemispheres
Focal deficits, h/a, seizures
Non-infiltrating (children)
Usually cerebellum, 3rd ventricle
Slow growth, minimal symptoms, easily resected
Oligodendroglioma & Ependymoma tumors
- Oligodendroglioma (middle adult)
Usually cerebral hemispheres white matter
Unpredictable, prone to hemorrhage - Ependymoma (young adult)
Epithelial lining of 4th ventricle/spinal canal
Hydrocephalus, increased ICP
Medulloblastoma tumor
Medulloblastoma
Originates in neurons of cerebullum, posterior fossa
Fast growing, spreads via CSF to brain/spine
Appears in infants, young children
Manifestations include signs of increased ICP
Highly malignant, but radiosensitive and excisable
Meningiomas
Outside brain, grows slowly
Older adult
Usually benign and excisable
Primary central nervous system lymphomas
Increased incidence of late
Common in immunocompromised
B-cell origin (lymphocytic)
Invasive, diffuse, aggressive
Brain Tumor Manifestations
Dependent on location and size Vasogenic edema/papilledema/increased ICP Headache – distinctive characteristics Often in the morning Improves with elevation of head Worse with sudden head movements Doesn’t respons to usual medications Accompanied by n&v Mentation changes Visual disturbances Focal signs seizures
Complex Partial seizure
Often temporal lobe Altered consciousness Hallucinations, déjà vu, idea flood, fear, etc. Automatisms Repetitive non-purposeful movements Contusion after is common
Secondarily Generalized Partial
Focal onset but generalized
Tonic/clonic activity, may have aura
Myoclonic generalized seizure
Brief muscle contractions bilaterally
Face, trunk or one or more extremities
Tonic
- rigid, violent contractions
Clonic
- Repeated contraction/relaxation
Tonic clonic generalized seizures: phases
Tonic Phase
Extension of extremities, loss of consciousness, incontinence, cyanosis
Clonic Phase
Rhythmic contraction/relaxation
Postictal Phase
Return to consciousness once RAS functions
