cns

Question 1

Cells of the brain

Answer 1

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

Question 2

Developmental Disorders

Answer 2

Dysraphic malformations (incomplete closure of neural tube): depending on the level of the defect - 
Anencephaly
Spina bifida
Meningocele
Meningomyelocele

Question 3

Anencephaly

Answer 3

Absence of cranium and cerebellum
Usually stillbirths
(like spina bififida but in the brains
still birth

Question 4

Spina bifida

Answer 4

Defect in the closure of vertebral arches

in spinal cord- completely curable

Question 5

Meningocele and Meningomyelocele

Answer 5

(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

Question 6

IntraCranial Hæmorrhages

Answer 6

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

Question 7

the 4 type of intracranial haemorrhages

Answer 7

Epidural
Subdural;
Subarachnoid
Intracerebral

Question 8

Epidural Hematoma!!! worst one usually kills the patient!!

Answer 8

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

Question 9

Subdural Hematoma

not good but better than epidural

Answer 9

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

Question 10

edema

Answer 10

can cause pressure in the intercranial , increates the oncotic pressure in the blood to draw the protein out

Question 11

Subarachnoid Hæmorrhage

Answer 11

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

Question 12

IntraCerebral Hæmorrhage

Answer 12

Blunt or penetrating trauma to head
Stroke

gun shot

exam what are the different types, what causes then- vein artery trauma

Question 13

Cerebrovascular Disease

Answer 13

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

Question 14

Stroke:Cerebral Infarct!!!!!

Answer 14

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

Question 15

Stroke: Intracerebral Hæmorrhage

Answer 15

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)

Question 16

Pathologic and Clinical features

Answer 16

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

Question 17

Prion Infection

Answer 17

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

Question 18

Creutzfeld-Jacob Disease

Answer 18

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.

Question 19

Demyelinating vs Degenerating diseases

Answer 19

Demyelinating diseases
Myelin loss
Loss of oligodendrocytes

Example: Multiple sclerosis (glial cells)

Degenerating diseases
Loss of neurons

Prototype: Alzheimer’s disease

Question 20

Multiple sclerosis

Answer 20

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

Question 21

Clinical features of ms

Answer 21

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

Question 22

Pathogenesis of MS

Answer 22

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)

Question 23

Alzheimer’s Disease

Answer 23

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

Question 24

Pathologic basis of symptoms of alzheimers

what does it look like

Answer 24

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

Question 25

Pathologic features of alzheimers

Answer 25

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

Question 26

Clinical Features and Diagnosis

Answer 26

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