ALTERATIONS IN NEURAL FUNCTION
I Disorders of the Brain
A. Mechanisms of Injury
1. Hypoxia
a. chronic vs. acute
2. Ischemia
a. global vs. focal
2. Excitotoxicity
a. glutamate and NMDA receptors
1. “calcium cascade”
2. mitochondrial disruption
3. Increased Intracranial Pressure (ICP)
a. cranial vault contents
b. Munroe-Kellie hypothesis (reciprocal compensation)
1. CSF flow
2. blood flow
a. subarachnoid veins vasoconstrict
b. systemic vasoconstriction to increase BP
c. cerebral perfusion presssure (CPP)
1. CPP = MAP - ICP
3. brain tissue compliance
a. herniation
1. compartments
c. intra-cranial pressure monitoring
When you have finished studying this material you should be able to:
- list the three general mechanisms causing brain injury
- distinguish between hypoxia and ischemia
- list causes of hypoxia and distinguish between chronic and acute hypoxia and their effects on the brain
- list typical causes of ishcemia and distinguish between focal and global ischemia and their effects on the brain
- define excitotoxicity, glutamate, NMDA receptors
- describe the events leading to excitotoxicity and the role of Ca+ in the toxicity
- define normal intracranial pressure (ICP) and list the major dangers of increasing this pressure
- describe the connection between trauma and ICP rise
- list the "compartments" of the cranial vault and explain "reciprocal compensation" (Munroe-Kellie Hypothesis) between these compartments
- explain the differences in compliance between the "compartments"
- define cerebral perfusion pressure (CPP), mean arterial pressure (MAP), herniation
- describe the early reciprocal compensations as ICP rises
- explain the causes for the rise in blood pressure as ICP rises
- explain the effects of hypoxia on the vessels in the brain and how this affects ICP
- explain why hyperventilation can be helpful as ICP rises
- list some of the symptoms accompanying a rise in ICP and explain the reason for these symptoms
- explain the connection between increased ICP and herniation
- explain how ICP can be monitored
B. Cerebrovascular Accidents (CVAs)
1. Characteristics
2. Types
a. Ischemic
1. thrombolytic stroke scenario
a. arteriosclerosis or arteritis
b. thrombus --> stenotic lesion
c. TIA (transient ischemic attack)
1. neurologic deficits
2. etiology
d. “stroke in evolution”
1. hypotension effect
2. embolytic stroke
a. etiology
b. onset
3. ischemic effects on tissue
a. infarct ---> penumbra
b. cytotoxic edema
c. vascular dysfunction
d. vasogenic edema
e. increased ICP, decrease CPP, herniation
f. recovery period
1. time
2. tissue repair
b. Hemorrhagic
1. characteristics
2. etiology
a. chronic hypertension
b. ruptured aneurysm
1. saccular
2. fusiform
c. arteriovenous malformation
3. effects on brain tissue
When you have finished studying this material you should be able to:
- define CVA and the diagnostic signs
- define thrombus, embolus, arteriosclerosis, atherosclerosis, arteritis, stenotic lesion
- distinguish between a TIA and a CVA
- contrast the timing of onset of a thrombolytic, an embolytic, and a hemorrhagic CVA
- list the sequence of events leading to an ischemic event
- explain why some ischemic events cause muscle weakness and others may cause a visual disturbance
- discuss the reason most thrombolytic CVAs occur during sleep
- list the most likely origins of an embolus and the "path of least resistance"
- define infarct, penumbra, cytotoxic edema, vasogenic edema
- explain why the loss of function right after a CVA is greater than can be explained by the infarct (dead cells)
- explain how an ischemic event can result in decreased cerebral perfusion
- identify the type of necrosis that occurs in the CNS, the glial cells involved and their role
- define xanthochromia, hematoma, aneurysm, arteriovenous malformation
- list the three major causes of a hemorrhagic CVA
- describe the effects of hemorrhagic CVAs and how they can lead to decreased cerebral perfusion
- compare and contrast berry aneurysms and fusiform aneurysms
C. Seizures
1. definition
2. epileptogenic focus
3. causes
a. primary (idiopathic), epilepsy
b. secondary (provoked)
4. types
a. partial
1. focal
2. prodroma
b. complex partial to secondary generalized
1. temporal lobe
2. automatisms
3. post-ictal confusion
c. generalized
1. both hemispheres
2. types
a. absence
b. atonic
c. myoclonic
d. tonic-clonic
5. metabolism
6. status epilepticus
D. Infections and Inflammations of CNS
1. Blood-brain barrier
2. Meningitis
a. bacterial (purulent)
1. pathophysiology
2. Haemophilus influenzae
b. viral (non-purulent)
3. Encephalitis
4. Creutzfeldt-Jakob Disease
E. Dementias
1. definition
2. Alzheimers Disease (AD)
a. etiology
b. manifestations
c. histology
1. BAP
2. neurofibrillary tangles
d. acetylcholine
e. treatment modalities
1. cholinergic agonists
2. acetylcholinesterase inhibitors
f. relationship to trisomy 21
F. Degenerative disease
1. Parkinsons Disease (PD)
a. extra-pyramidal system
b. “release phenomenon”
c. manifestations
d. dopamine vs. acetylcholine
G. Developmental Abnormalities
1. Neural development
2. Spina bifida occulta
3. Spina bifida cystica : meningocele and myelomeningocele
When you have finished studying this material you should be able to:
- define seizure, epileptogenic focus, epilepsy, post-ictal, atonic, myoclonic, tonic-clonic, status epilepticus
- distinguish between primary and secondary seizures and some causes of each
- list the three types of seizures and compare their sites of activity, effects on consciousness, and seizure behaviors
- explain the danger of status epilepticus
- explain why infections are less common in the CNS and harder to cure if they reach the CNS
- diagram a crossection of the blood brain barrier and explain how it was originally discovered
- distinguish between bacterial meningitis, viral meningitis, encephalitis, and Creutzfeldt-Jakob disease including causative agents
- explain why bacterial meningitis spreads so rapidly, involves edema and thickened CSF, and may precipitate thromboses
- identify the age group at risk for Haemophilus influenzae and the route it takes to reach the brain
- define dementia and list some conditions in an elderly person which could be misdiagnosed as dementia
- identify the most common cause of dementia and its etiology
- distinguish between aphasia, apraxia, and agnosia
- compare neurofibrillary tangles, BAP and amyloid plaques
- explain why someone with Trisomy 21 is likely to develop dementia
- state the neurotransmitter deficiency correlated with Alzheimer's Disease and one possible way to compensate for the deficiency
- describe the areas of the brain involved in Parkinson's Disease and the neurotransmitter used by these areas
- compare pyramidal and extrapyramidal motor tracts by their locations and roles and the tracts involved in Parkinson's Disease
- describe the "release phenomenon" and the dyskinesias of Parkinson's Disease
- explain the connection between dopamine and acetylcholine and these dyskinesias
- define neural tube (in development), spina bifida, spina bifida occulta, meningocele, myelomeningocele
- identify the most common sites of these abnormalities and the resulting impairments
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