Week 5- Lecture 1b - Alterations in Central Nervous System Function

Question 1

What is included in the forebrain

Answer 1

telencephalon - cerebral cortex, basal ganglia, hippocampus, amygdala

diencephalon - thalamus, hypothalamus, epithalamus

Question 2

what is included in the midbrain

Answer 2

mesencephalon - tectum, tegmentum

Question 3

What is included in the hindbrain

Answer 3

cerebellum, pons, medulla

Question 4

4 brain protection

Answer 4

bone (skull)
membranes (meninges)
Watery cushion (CSF)
BBB - helps maintain stable environment or the brain - separates neurons from blood borne substances such as hormones and neuro transmitters

Question 5

CSF composition

Answer 5

watery solution formed from blood plasma - less protein and different ion concentrations than plasma

Question 6

Functions of CSF

Answer 6

gives buoyancy to CNS structures

protects CNS from blows and other trauma

nourishes brain and carries chemical signals

Question 7

What is the choroid plexus

Answer 7

hang from the roof of each ventricle

• clusters of capillaries enclosed by Pia mater and layer of ependymal cells
• produce CSF at constant rate
• keep it in motion

ependymal cells

• use ion pumps to control composition of CSF
• help cleanse CSF by removing wastes

normal volume of CSF 150ml

• replaced every 8 hours
• 500ml formed daily

Question 8

BBB function

Answer 8

helps maintain stable environment for brain and separates neurons from some blood borne substances

Question 9

BBB composition

Answer 9

continuous endothelium of capillary walls

thick basal lamina around capillaries

feet of astrocytes

• provide signal to endothelium for formation of tight junctions
• tight junctions complete, forming blood brain barrier

Question 10

BBB function outlined

Answer 10

The blood brain barrier is a selective barrier that allows nutrients to move by facilitated diffusion. As it’s role is to maintain a stable environment for the brain, it denies metabolic wastes, proteins, most drugs, small nonessential amino acids and K+. Alcohol, nicotine and anaesthetics are all substances that are allowed to pass due to their fat solubility

Question 11

BBB is absent in some areas - why?

Answer 11

the blood brain barrier is absent in areas like the hypothalamus and the vomiting centre. This is so hypothalamus can monitor water balance, temperature and metabolic activity of the body. The vomiting centre monitors for poisonous centres

Question 12

Neuronal injury response is dependant on

Answer 12

the specific cell type involved

Question 13

Support cells injury responses

Answer 13

astrogliosis
microgial nodules
ependymal damage which leads to CSF alterations

Question 14

Injury responses of neuron

Answer 14

neuropathy
axonal damage
demyelination

Question 15

Astrogliosis

Answer 15

Astrogliosis is where an astrocyte responds to local injury by the process of proliferation (forms a glial scar)

Contusions, wounds, tumours, abscesses, hemorrhages are all common causes of tissue injury that elicit an astrogliosis response

Unchecked proliferation can lead to neoplastic transformation (glioma - brain cancer)

Question 16

MOIs of CNS injury

Answer 16

Traumatic CNS injury
Ischemic CNS injury
Excitation injury
CNS pressure injury

Question 17

Microglial

Answer 17

Has an immune response, reactive changes include nucleus extension ( rod cells)
Can join to astrocytes to form microglial nodule - brain contains very few lymphocytes - T-Lymphocites do not cross BBB

Question 18

Ependymal cell damage response

Answer 18

CSF production transfer is altered with ependymal cell damage due to infection of ventricles and intraventricular haemorrhaging

Question 19

Traumatic CNS injury

Answer 19

can have impaired neurologic functioning which can either be local or systemic (usually always systemic )

In terms of a local effect, this injury is to neuronal tissue transmitting signals to a specific area

A systemic effects involves injury to a site responsible for integrating transmission of impulses to multiple distant sites (usually CNS)

Question 20

TBI aka concussion

Answer 20

MOIs include automobile accidents, falls, sports related injuries and “shaken baby syndrome”

TBIs can lead to changes in physical, intellectual, emotional and social abilities.

Can be categorised as closed head injury and open traumatic injury

Question 21

Closed head injury

Answer 21

involves movement of the brain inside of the skull causing the injury

Question 22

Open traumatic injury

Answer 22

involves exposure of brain structures such as the meninges and brain tissue

with this comes the risk of infection and also risk of further injury

Question 23

Traumatic brain injuries

Answer 23

With traumatic brain injuries comes a lot of complications, these include increased seizure activity, concussion (which has temporary alterations in function -dizzy/unconscious), contusions (which has permanent damage - cortical contusions - may remain conscious
- brainstem contusions - always cause coma / injury to the reticular activiting system (RAAS)

Other complications include hepatomas, oedema, skull fractures, increased ICP, respiratory depression, Brain hernias

Question 24

Diagnosis of TBIs

Answer 24

diagnosis tools for traumatic brain injury include
imaging modalities ( CT, MRI)
EEGs for brain activity
Lumbar puncture (spinal tap) : for analysis of CSF and check presence of blood (intracranial haemorrhaging)

Question 25

Treatment for TBIs

Answer 25

Treatment for TBI's is targeted towards the specific injury surgery can be performed to evacuate haematomas removal of foreign fragments Reduce intracranial pressure (ICP) Pain control anticonvulsive medication (prevent seizures) Respiratory support Antibiotics to prevent infection

Question 26

SCI

Answer 26

``` most SCI's are among males - may be result of fractures -contusions -compression of the vertebral column -trauma to the head or neck ``` neurologic damage is the result of - pulling - twisting - severing - compressing the neural tissue of the spinal cord

Question 27

Different spinal cord injuries

Answer 27

lacerations - rip or tear from vertebral fracture, knife or bullet transection : completely severed, penetrating trauma incomplete transection contusion: falls, acceleration/deceleration injury compression : crushing distraction : pulling spinal cord apart (top moved while bottom fixed)

Question 28

Clinical manifestations of vertebrae fracture

Answer 28

localised pain

Question 29

clinical manifestations of SCI

Answer 29

wide range - from mild paresthesia (abnormal sensation) to quadriplegia (paralysis of all four extremities) - level of SCI and severity contributes to neurologic deficit

Question 30

Diagnosis for a traumatic SCI

Answer 30

X-ray for fractures neuro examination lumbar puncture CT, MRI

Question 31

Treatment for traumatic SCI

Answer 31

immediate immobilisation to prevent further injury corticosteroids to lessen inflammation further treatment : traction , casting, surgery

Question 32

ischaemic central nervous system injury

Answer 32

inadequate perfusion to neurologic tissue - impaired oxygenation - tissue necrosis cause of ischemia 1. local ischemia (specific region of the brain - occlusion of blood supply by thrombosis in a local vessel 2. global ischemia (larger areas of CNS affected - inadequate blood supply to meet the needs of brain tissue - global ischemia spinal cord ischemia : occlusion of spinal blood vessels

Question 33

6 steps of an ischemic CNS injury

Answer 33

1. impaired blood flow lasting longer than a few minutes 2. brain tissue infarction occurs 3. cellular function ceases because of inability to use anaerobic processes or uptake glucose and glycogen 4. infarction stimulates response to tissue injury that leads to inflammation 5. inflammatory response leads to oedema development 6. Oedema leads to increased intracellular pressure (ICP) cell injury also cause local water, electrolyte imbalances and acidosis - calcium, sodium, water build up - free radical formation at injury site - increased release of excitatory neurotransmitter (glutamate)

Question 34

clinical manifestations of iscaemic CNS injury

Answer 34

sensory and motor functions are often affected If injury in brain : manifestations reflect specific associated functions with motor deficits on contralateral side loss of consciousness, weakness, difficulty speaking, impaired vision , paresthesia

Question 35

diagnosis for Ischaemic CNS injury

Answer 35

CT, MRI, angiography to diagnose ischaemic blockage | PET scan: altered metabolism in surrounding tissue

Question 36

treatment for ischaemic CNS injury

Answer 36

manage ICP restore perfusion thrombolytic therapy to dissolve clot anticoagulation therapy to prevent future clot

Question 37

excitation injury

Answer 37

pathologic consequences of increased impulse frequency, intensity, cascade of transmission glutamate is the main excitatory neurotransmitter - involved numerous higher order function - glutamate binds to its receptor on postsynaptic membrane (many types of receptors) - NMDA: N-Methyl-D-aspartate receptor is one subtype with affinity for glutamate signal transduction initiated IF : high levels of glutamate binds to NMDA, leads to prolonged action potentials Prolonged action potentials leads to protein breakdown, formation of free radicals, DNA damage, breakdown of nucleus

Question 38

excitation injury cont'

Answer 38

may result from cell inability to meet metabolic demand - oxygen needs increase with increased neurologic activity - risk of hypoxia increased - if ischaemia is present, more glutamate Is released by the cells - excitation is intensified by binding to NMDA receptor tissue sensitive to hypoxia may suffer from permanent damage - hippocampus - cerebral cortex

Question 39

manifestations of excitation injury

Answer 39

reduction in higher order function | cognitive and memory abilities

Question 40

Excitation injury cont' #2

Answer 40

cell death from glutamate may be prevented - effects can be blocked - excessive level can be removed from synapse glutamate has wide range of involvement in normal cell functioning pharmacological blocking is difficult during periods of deteriorating brain functions excitatory responses may predominate severe brain injury difference is based on the injury site impacted CNS involvement A . flexor or decorticate posture - damage to cerebral hemispheres above midbrain B extensor or decerebrate posture -damage to midbrain, brainstem

Question 41

CNS pressure injury

Answer 41

skull and vertebral column : rigid structure - restricted expansion ``` increase in pressure may result in injury : increased intracranial pressure cause : 1. excessive CSF volume 2. cerebral oedema 3. Space occupying lesion (tumour) ```

Question 42

CNS pressure injury

Answer 42

excessive CSF volume increased production decreased absorption - obstruction of the ventricular system - obstruction may occur through inflammation, tumour, haemorrhaging or a congenital anomaly CSF build up in the ventricles leads to dilation of ventricles

Question 43

CNS pressure injury

Answer 43

oedema - abnormal water accumulation - vasogenic oedema : transfer of water and protein from the vascular to interstitial space (following permeability change, pressure change) - Cytotoxic oedema : caused by hypoxia secondary to ischaemia - cellular swelling manifestations - altered consciousness - intracranial hypertension - neurologic deficit

Question 44

CNS tumour can promote pressure injury

Answer 44

may obstruct CSF flow promote brain displacement (brain herniation) to lower pressure area - stimulation of vomiting centre of medulla : nausea -personality challenges, memory loss, depression

Question 45

increased ICP

Answer 45

common response to pathologic events is increased intracranial pressure - leads to blood flow reduction - ischemia - death of brain cells - damage to brain structure - functional loss manifestations of increased ICP - headache - vomiting - papilledema (oedema of optical disk) - mental deterioration

Question 46

treatment of ICP

Answer 46

excessive CSF : surgical shunting from intraventricular spaces - to peritoneum : ventriculoperitoneal shunt - to right atrium : ventriculoatrial shunt - catheter -- left ventricle -- internal jugular vein -- right atrium Cerebral oedema - osmotic diuretics - fluid removal and excretion