cns Flashcards
Cells of the brain
Neurons (non regenerated) (neuroplasticity- if a damged area then other areas can compensate)
Neocortex, cerebellum, cranial nerve nuclei
Glial cells (can form a scar in tissue - glyocist, meningial tissue can have the scars- can trigger epilepsie- healing in itself can cause pathology)
Astrocytes, oligodendrocytes, ependymal cells and microglial cells
Major function is to support the neurons and oligodendrocytes produce mylein
Developmental Disorders
Dysraphic malformations (incomplete closure of neural tube): depending on the level of the defect - Anencephaly Spina bifida Meningocele Meningomyelocele
Anencephaly
Absence of cranium and cerebellum
Usually stillbirths
(like spina bififida but in the brains
still birth
Spina bifida
Defect in the closure of vertebral arches
in spinal cord- completely curable
Meningocele and Meningomyelocele
(2 different kinds of spina bifida)Lack of fusion of posterior bony arch
Protrusion of meninges through defect
Protrusion of meninges and part of spinal cord
IntraCranial Hæmorrhages
Anatomy Cranium Meninges Dura mater (first layer -on the brain) Arachnoid (blood vessels- 2nd layer) Pia mater (third layer, thick) Cerebrum 4 types Epidural !!! Subdural; Subarachnoid Intracerebral
Major problem is increased intracranial pressure
the 4 type of intracranial haemorrhages
Epidural
Subdural;
Subarachnoid
Intracerebral
Epidural Hematoma!!! worst one usually kills the patient!!
Between skull and dura mater
Ruptured meningeal artery branch!!! (usually caused by skull fracture) (only have a few seconds to control it so cannot get medical attention fast enough)
Progresses relatively quickly – consciousness usually lost rapidly
As space-occupying lesion, will compress brain & cause coma & death
Subdural Hematoma
not good but better than epidural
Between dura & arachnoid Thin-walled veins!!!!! (leaks out slower so more time, some times so small dont even notice), torn by blunt trauma (boxing , blow, shaking) Symptoms may be non-specific (headache) Progresses relatively slowly May cause coma and death if untreated
boxing and alcoholism is the causes
happens to alcohol when walking
edema
can cause pressure in the intercranial , increates the oncotic pressure in the blood to draw the protein out
Subarachnoid Hæmorrhage
Between arachnoid & pia
Traumatic contusion of brain (multiple blows to the head- beating up)
Ruptured aneurysms of circle of Willis
1–2 % of population
Hypertensive or spontaneous (berrie aneurism- thin walls can burst when high blood pressure
IntraCerebral Hæmorrhage
Blunt or penetrating trauma to head
Stroke
gun shot
exam what are the different types, what causes then- vein artery trauma
Cerebrovascular Disease
3rd most common cause of death Disease of old age Related to: Atherosclerosis of cerebral arteries Hypertension Thromboembolism Usually due to (both together referred to as STROKE) Cerebral infarction Intracerebral hemorrhage
neurons die and do not regenerate
Stroke:Cerebral Infarct!!!!!
Presents as stroke
Symptoms depend on the area infarcted
Usually thrombosis of atherosclerotic artery (carotids, cerebral circulation)
Area infarcted depends of location of blockage
Ischemic brain liquefies
(encephalomalacia) – Liquefactive necrosis
Edema surrounds the area – reversible damage
parts of the brain can die - death of the neurons- leads to edema by trying to repair which causes more damage
Stroke: Intracerebral Hæmorrhage
Usually hypertensive Usually intense (damaging the small blood vessels) headache Common sites Basal ganglia (2/3) Cerebellar Pontine
(important to distinguish what type of stroke the patient has- classification - worst headache in your life)
Pathologic and Clinical features
Well-circumscribed hematoma, surrounded by edematous tissue
Reversible damage- edema
Transforms into pseudocyst (yellow fluid)
Resemble traumatic hæmorrhage
More dramatic
30% lose consciousness
Others complain of severe headache or nausea
E.g. Basal Ganglia hemiplegia ± hemiparesis
Prion Infection
Small infectious protein particles
Previously called “slow-viruses” (infectious period of years before signs or symptoms)
Infect CNS selectively by direct exposure
Kuru – infection spread by eating the brains (??) of infected individuals
BSE (bovine spongiform encephalitis or “mad cow disease”)- abnormaly folded protein that you eat goes to your brain- found in all game meat too but it does not affect us
Creutzfeld-Jacob disease (CJD)- just skin and bones- really thin- domino effect of changin the form of proteins- improper transcription - folds abnormally so can be genetically passed down
kuru: new guinea ppl were eating brains- the men were eating it but the women were getting the disease - forms abnormaly folded proteins
Creutzfeld-Jacob Disease
Early on, brain is normal; later-> brain atrophy
Hallmark: vacuolization of cells (wholes everywhere, eventually can destroy neurons as it increases in size) of grey matter (spongiform change) with neuronal loss
Rapid disease progress once signs/ symptoms appear – (DEMENTIA): death within 30 days to several months.
Demyelinating vs Degenerating diseases
Demyelinating diseases
Myelin loss
Loss of oligodendrocytes
Example: Multiple sclerosis (glial cells)
Degenerating diseases
Loss of neurons
Prototype: Alzheimer’s disease
Multiple sclerosis
Classic history
Recurrent / Relapsing neurologic deficits
(b lymphocyes come and destroy the myelin- then the macrophages come in and eat the myelin)- astrocytes then come in and fill in the space
Pathologic basis of symptoms
Plaques: areas of demyelination in the white matter
Multiple
Focal
Clinical features of ms
Location of the plaques will determine the main symptoms and signs (both motor and sensory symptoms) Brain Optic nerve Angles of lateral ventricles Spinal cord
Pathogenesis of MS
Short answer: Don’t know
(dont need to know) Factors considered important
Autoimmune basis
More common in women (2:1),
Environmental factors: in temper$ate climates (1:1000 in N.A.);
Genetics may play a role (15 times more common in first degree relatives)
DIAGNOSIS OF MS!!!!!
History and Physical: two sets of CNS symptoms in two!!! episodes!!!
Lumbar puncture: an increased level of IgG and the presence of oligoclonal bands in the CSF.
Radiography: MRI; CT (abnormal signals in the periventricular white matter)
Alzheimer’s Disease
Classic cause of isolated!!! (no association with anything else like leg pain as well as lost memories) dementia
Other causes of dementia would have clinical clues
Incidence:
Older people > 70 years
50-60% of people > 85 years
Unknown
Genetic factors
Familial linked to chromosomes 19 & 21
Carriers of Apo E4 gene develop Alzheimer’s frequently
Pathologic basis of symptoms of alzheimers
what does it look like
Neuronal loss (global atrophy!!!!!! of the brain)
the spaces between the nouddle like part of the brain are bigger, leads to a very light brain
Pathologic features of alzheimers
Neurofibrillary tangles!! (abnormally folded- grows without being estroys)
Intracytoplasmic bundles of microtubular filaments (TAU protein)
Senile (neuritic) plaques (different than ms- abnormal accululation of amyloid)
Degenerated nerve cell processes surrounding an amyloid core (plaque core is Abeta protein derived from APP)
Amyloid angiopathy
Amyloid in small intracerebral vessels
- problems with circulation
2 protein and blood vessels
Clinical Features and Diagnosis
Dementia (progressive loss of cognitive functions)
Functional decline
interferes c Work
Loss of memory progresses to completely dysfunctional patient (bed-ridden)
Definitive diagnosis requires pathologic examination of brain tissue
Combination of clinical assessment and radiologic methods allows diagnosis in 80-90% cases
inappropriate responses- crying…
only way for 100% diagnoses is through autopsie
psychosocial aspect- do worse in nursing homes
