Nervous Flashcards
Describe the pathophysiology of Stroke and Transient Ischaemic Attack
Sudden Neurological deficit caused by:
- vascular occlusion from thrombosis or embolism. Most are caused by an Emboli that separates from a thrombus in a large vessel such as the carotid artery, then travels distally, where it lodges in a brain vessel and results in an infarct/blockage.
Most thrombi initially form because the endothelium of the vessel in which they arise has been damaged by atherosclerosis.
Consequently, the common denominator of most CVA is atherosclerotic vascular disease, and is why CVA become more prevalent in older adults.
Whether from emboli/thrombi, vascular occlusion results in infarcts of the brain tissue supplied by the vessel.
Damaged brain tissue loses function within minutes, and becomes soft and necrotic within a few days. Later the tissue is lost from the area, leaving a cystic cavity.
Middle Cerebral Artery is most often occluded by emboli as it is a direct continuation of carotid artery, and is important as it supplies the part of the cortex controlling motor function. It can cause weakness (paresis) or paralysis on the opposite side of the body.
If dominant side of brain(usually Left) which controls speech and motor function, is affected, pt will also suffer impaired language function(aphasia).
CVA involving vertebral arteries or their branches may also cause paralysis because of injury to the motor fibres in the brain stem coursing between the brain and spinal cord.
Large CVA in the brain stem usually kill a pt because of interruption of the nervous centres that control respiration. - haemorrhage into the brain from a ruptured blood vessel. The vessel has usually been weakened by arteriosclerosis, most often in pt with hypertension. Signs and symptoms depend on location and size, up to half of pt with large haemorrhage die within hours, as the accumulation of blood displaces adjacent tissue and rapidly increases intracranial pressure.
- ruptured Saccular(berry) aneurysms. Mainly found to be in vicinity of the Circle of Willis where the blood vessels branch. They are saccular outpouchings of vessels caused by deficiencies in the vessel wall. When they rupture, blood is spilled into the sub-arachnoid space and can be detected in the cerebrospinal fluid, meaning that if this is analysed it can distinguish these from other types of stroke.
Deprivation of blood to a body tissue(Ischemia), impairs the deliver of oxygen and nutrients. The critical long term effect of a CVA/Stroke is that In brain tissue the neurons that are deprived of oxygen die within minutes to hours and are never replaced. When this occurs they release an overabundance of Glutamate(an excitatory neurotransmitter), this excites the surrounding cells until they die.
High levels of calcium ions damage mitochondria of brain cells and initiate specific protein synthesis to cause cell death via free radicals and inflammatory agents.
Oligodendroglia are also very vulnerable to injury and readily die following ischemia.
Astrocytes multiply rapidly and repair the injury structurally by forming a scar.
Monocytes enter from the blood after injury and aid in clearing away the debris.
Treatments include plasminogen activator to dissolve blood clots, and robotic surgery.
Temporary episodes of cerebral ischemia are known as Transient Ischemic Attacks, they can last between 5 and 50 mins, causing temporary paralysis, numbness or speech impairment
Describe the pathophysiology of Meningitis
Meningitis is an inflammation of the membranes covering the brain and spinal cord(Meninges).
Most commonly bacterial, which is communicable through droplet transmission, not through air.
Transmission occurs following direct contact with nasopharyngeal secretions, eg. mouth to mouth, spray from suctioning/intubation.
The bacteria usually gain access to the brain and spinal cord via the blood.
Most commonly implicated bacteria are:
- Neisseria Meningitidis
- Streptococcus pneumoniae
- Haemophilus influenzae
- group B Streptococcus
- Listeria Monocytogenes
Also viral, which is non-communicable.
Meningococcal meningitis is the type that is most often involved in epidemic outbreaks, that can occur at any time and affect mainly pt’s in their late teens. It’s incubation period is between 2 and 10 days. Sporadic cases occur most frequently during winter and spring
Communicable period is variable - as long as meningococcal bacteria are present in pt nasal/oral secretions.
Non specific Signs/Symptoms make diagnosis difficult:
- Fever
- Nausea/vomiting
- Lethargy
- Irritability/unsettled state
- Ill appearance
- Refusing food/drink
- Headache
- Muscle ache/joint pain(particularly neck stiffness)
- Respiratory signs/symptoms
- Seizures
- Coma
Diagnosis made on basis of cerebrospinal fluid findings from lumbar tap:
- neutrophilic leukocytes
- decreased glucose
- presence of organisms
Treatment is antibiotic therapy.
inadequate or non-immediate treatment results in alterations to or breakdown of the blood-brain barrier, leading to oedema with consequent increase of intracranial pressure and death of the pt.
the lesion of acute meningitis is mainly purulent exudate in the subarachnoid space.
less commonly the bacteria settle in the brain parenchyma rather than the meninges, and form an abscess that behaves as an expanding mass lesion, and if untreated, almost always causes death.
Chronic meningitis may be caused by tuberculosis or several types of fungal organisms, commonly Cryptococcus neoformans.
Inflammatory cells in chronic meningitis are monocytes and lymphocytes rather than neutrophils. The disease often solders at the base of the brain for weeks to months, gradually affecting more and more cranial nerves at their point of exit from the brain.
If a pt does not die from acute or chronic meningitis, there is danger of developing hydrocephalus from the obliteration of the subarachnoid space by fibrous tissue, resulting in the failure to absorb cerebrospinal fluid.
Chronic meningitis can also accompany Lyme disease, histoplasmosis, and blastomycosis
Describe the pathophysiology of raised intracranial pressure in relation to head injuries
In adults the skull is a rigid protective barrier around the brain, that allows little if any expansion of the intracranial contents.
An injured brain starts to swell due to cerebral vasodilation, then an increase in cerebral water(cerebral oedema) contributes to further brain swelling.
Accumulation of blood within the skull or swelling of the brain can rapidly lead to increase in Intracranial Pressure(ICP), pressure within the cranial vault.
Increased ICP squeezes the brain against bony prominences within the cranium.
Normal ICP in adults ranges from 0-10 mm Hg.
Increase in ICP from the likes of cerebral haemorrhage or cerebral oedema, decrease cerebral perfusion pressure and cerebral blood flow.
Cerebral Perfusion Pressure(CPP), the pressure of blood flow through the brain, is the difference between the Mean Arterial Pressure(MAP)(average pressure against arterial wall during a cardiac cycle) and the ICP.
Decrease in cerebral blood flow is potentially catastrophic as the brain depends on a constant supply of blood to provide its oxygen and glucose needs, for survival.
The Critical Minimum Threshold, or minimum CPP required to adequately perfuse the brain is 60 mm Hg in an adult. Any less can result in cerebral ischaemia, and possibly neurological impairment or death.
The body responds to a decrease in CPP by increasing MAP, resulting in cerebral vasodilation and increased cerebral blood flow, a process called ‘Autoregulation’.
However, this increase in cerebral blood flow, causes a further increase in ICP, and as ICP increases CSF is forced from the cranium into the spinal cord.
Pt with raised ICP is caught in vicious cycle:
- as ICP increases
- cerebral blood flow increases, secondary to autoregulation
- leading to potentially fatal increase in ICP
Conversely, if cerebral blood flow decreases, CPP decreases as well, and the brain becomes ischaemic.
If ICP is not treated promptly, cerebral herniation may occur, where the brain is forced from the cranial vault, either through the foramen magnum or over the tentorium.
Clinical signs of ICP depend on the amount of pressure inside the skull and the extent of brain stem involvement.
Early signs/symptoms:
- vomiting(often without nausea)
- headache
- altered level of consciousness
- convulsions
Later signs/symptoms: - hypertension(with widening pulse pressure) - bradycardia - irregular respirations (CUSHING'S TRIAD)
- unilaterally unequal and nonreactive pupil(oculomotor nerve compression)
- coma
- posturing: decorticate(flexor) - flexion of arms and extension of legs, decerebrate(extensor) - extension of arms and legs.
Describe the pathophysiology of primary spinal cord injuries
This describes the pattern of damage that occurs at the time of injury and is often related to 2 distinct mechanisms:
- penetrating trauma - typically results in complete or partial cord transection.
- blunt trauma - may displace ligaments and bone fragments, resulting in compression of points of the spinal cord or an incomplete dislocation of the vertebral body.
in summary 3 common abnormalities can be sustained:
- destruction from direct trauma
- compression by bone fragments, haematoma, or disk material
- ischemia from impingmentof, or damage to, spinal arteries
Spinal cord concussion, characterised by temporary dysfunction, lasts 24-48 hours. It is a transient disturbance of spinal cord function and is considered an incomplete injury.
Spinal cord contusion can occur with/without vertebral damage or without demonstrable pathological changes. These injury patterns may result from a rapid change in velocity following trauma.
Cord laceration usually occurs when a projectile or bone enters the spinal canal, resulting in haemorrhage into the cord tissue, swelling, and disruption of some portion of the cord and its associated communication pathways.
Describe the pathophysiology of secondary spinal cord injuries
Occurs when multiple factors permit a progression of the primary spinal cord injury.
The resulting inflammatory responses may result in further deterioration.
Effects that can be exacerbated by by exposing neural elements to further hypoxaemia, hypoglycaemia and hypothermia.
Further injury should be minimised by stabilisation-restricting spinal movement, minimising heat loss and maintaining oxygenation and perfusion.
Following neurological examination SCI will be defined as:
- Complete SCI - complete disruption all tracts of the spinal cord, with permanent loss of all cord-mediated functions below the level of transection.
- Incomplete SCI - pt retains some degree of cord-mediated function.
Degree of SCI is best determined 24 hours after injury, as initial dysfunction may be temporary.
When the injury affects the cord in the cervical spine, tetraplegia may result, affecting all 4 limbs.
Paraplegia is said to exist when an injury occurs in the thoracic, lumbar, or sacral segments, resulting in impairment of legs and pelvic organs.
Describe the pathophysiology of Spinal shock
refers to the temporary, local neurological condition that occurs immediately after spinal cord trauma.
May last several hours to several weeks depending on the severity of the injury.
swelling of the cord can begin within 30 mins of initial injury and can lead to physiological transection, mechanically disrupting all nerve conduction distal to the injury.
pt may present with varying degrees of acute spinal injury. Potential findings: - flaccid paralysis - flaccid sphincters - absent reflexes
Findings:
- sensory function impaired below level of injury
- thermoregulation and visceral function below lesion
- bowel distension caused by loss of peristalsis
Describe the pathophysiology of Neurogenic Shock
refers to haemodynamic triad of hypotension, bradycardia and peripheral vasodilation with temporary loss of autonomic function resulting from SCI at or above the level of T6.
Marked haemodynamic and systemic effects are seen:
- hypotension occurs because of absent/impaired peripheral vascular tone with the loss of alpha receptor stimulation
- Blood pools in the dilated vascular space, causing a relative hypovolaemia and making the pt sensitive to sudden position changes
- decrease in cardiac preload associated with poor venous return results in a fall in stroke volume and cardiac output
- bradycardia results from unopposed vagal tone along with adrenal gland suppression from loss of sympathetic stimulation, resulting in adrenaline/noradrenaline suppression
- hypothermia and the absence of sweating are seen because the loss of sympathetic stimulation.
The classic case of neurogenic shock is a hypotensive, bradycardia pt whose skin is warm, flushed and dry below the level of the spinal lesion.
A pt with concomitant traumatic injuries may still demonstrate signs of hypovolaemic shock from external/internal blood loss, masking the signs of neurogenic shock.
Define Anterior cord syndrome
rare syndrome resulting from displacement of bony fragments into the anterior portion of the spinal cord.
often caused by flexion injuries or fractures.
the anterior spinal artery provides blood to the anterior 2/3 of the spinal cord, disruption presents as anterior cord syndrome.
findings:
- paralysis at or below level of injury
- loss of sensation to pain, temp and touch
Define Central cord syndrome
hyperextension injuries to the cervical area present with haemorrhage or oedema to the central cervical segments.
rarely associated with fractures/bone disruption.
more often occurs in conjunction with tears to the anterior longitudinal ligament.
frequently seen in older pt’s that may already have a significant degree of cervical spondylolosis and stenosis as a result of arthiritic changes.
brief episode of hyperextension can exert pressure on the spinal cord within the relatively diminished spinal canal.
within the central cord, motor fibres are distributed in a unique fashion with more cervical and thoracic motor and sensory tracts than in the periphery of the cord.
findings:
- greater loss of function in upper extremities
- variable loss of sensation to pain and temp
- bowel/bladder dysfunction
Define Posteror cord syndrome
associated with extension injuries.
relatively rare syndrome produces dysfunction of the dorsal columns.
findings:
- decreased sensation to light touch
- proprioception(the ability to perceive the position and movement of one’s own body)
- decreased perception of vibration
Most other motor and sensory functions remain intact.
Define Brown-Sequard syndrome
occurs when penetrating trauma is accompanied by hemitransection of the cord and complete damage to all spinal tracts on the involved side.
injury to the corticospinal motor tracts, causes motor loss on the same side(ipsilateral) as the injury, but below the lesion.
damage to the dorsal column causes loss of sensation to light touch, proprioception, and vibration on the same side but below the injury.
disruption of the spinothalamic tracts causes loss of sensation to pain and temp on the opposite side to the injury(contralateral), below the lesion.
Briefly describe the pathophysiology of senile dementia
descriptive term for a condition of older persons, having a decrease in cognitive function, usually accompanied by loss of/poor memory for recent events, pick at their clothes, get lost easily, often irritable.
degree of dementia is proportional to loss of substance in the frontal lobes, the region of the brain associated with higher cognitive function.
loss of substance may be the result of trauma or stroke(infarct), but is most often secondary to generalised atrophy and degeneration of the neutrons in the grey matter.
when accompanied by certain microscopic brain changes, it is known as Alzheimer disease.
characteristic silver-staining neuritic plaques and neurofibrillary tangles, as well as an abnormal protein called ‘amyloid’, are found in the cerebral cortex allowing a neuropathologist to diagnose Alzheimer disease.
a large number plaques, tangles and amyloid are found in the temporal lobes explaining the loss of recent memory associated with the disease.
it is not known what causes the neutrons to degenerate resulting in alzheimer disease, and there is no real effective treatment.
Briefly describe the pathophysiology of Parkinson’s
caused by degeneration of certain portions of the extrapyramidal(involuntary) motor system, especially the substantia nigra nucleus in the midbrain.
a characteristic inclusion called the ‘levy body’ is present in degenerating substantia nigra neurons.
usually, but not always, affects older people, resulting in:
- tremors at rest
- masklike facial expression
- shuffling gait
- rigidity of skeletal muscles
many older people appear to have minor degrees of Parkinson’s disease, and around half of people with parsons disease suffer some degree of dementia.
Briefly describe the pathophysiology of Multiple Sclerosis
the basic lesion is focal loss of the myelin sheath(demy-eli-nation), which appears to render the axons of a neutron incapable of transmitting a nervous impulse.
as this loss of myelin can occur anywhere in the brain or spinal cord, symptoms vary considerably.
Visual impairment is usually present to some degree as multiple sclerosis preferentially affects the optic nerves as well as the tissue surrounding the brain ventricles and the spinal cord.
cause is unknown, but strong suspicion that it is caused by a virus/immunologic reaction to a virus in persons that are genetically predisposed.
disease span is 2-25 years with the course of the disease alternately remitting and relapsing.
eventually pt’s become quite debilitated from muscle weakness.
diagnosis found on basis of clinical history and physical findings that support a multifocal neurologic deficit, plus the findings of increased immunoglobin G protein in the cerebrospinal fluid. Lesions can be seen using MRI.
Briefly describe the pathophysiology of seizures
also known as convulsions or fits.
focal/partial and/or generalised disturbances(sudden, erratic firing) of neuronal electrical activity, which may be manifested by abnormal movements or sensations and loss of reflexes, memory, or consciousness.
during a convulsion neutrons are in a hyper metabolic state(using large amounts of glucose and producing lactic acid). for short periods, this state does not cause long-term damage. if convulsions continue the body cannot remove the waste products effectively or ensure adequate glucose supplies. such a hyper metabolic state can result in neutrons being damaged or killed.
GENERALISED - affecting large portions of the brain:
- absence - staring/absent spell during which activity ceases, most common in children 4-12 years, typically less than 15 seconds, no postictal phase.
- tonic/clonic - LOC, muscle contractions, aura(warning), any age, lasts minutes, prolonged/ consecutive seizures(without lucid interval) termed status epilepticus.
FOCAL/PARTIAL - affecting limited area of the brain:
- simple partial convulsion - known as focal motor/jacksonian march convulsions, tonic/clonic activity localised to part of the body, may spread to rest of body, no aura or LOC.
- complex partial convulsion - known as temporal lobe or psychomotor convulsions, manifests as change in behaviour(mood change), aura, less than 1-2 minutes, pt quickly regains normal mental status, no postictal phase.
Causes:
- epilepsy(condition of recurrent seizures)
- electrolyte imbalance
- high fever(febrile convulsions)
- hypoglycaemia
- alcohol
- brain infections(meningitis)
- recreational drugs
- uraemia(kidney failure)
- eclampsia
- idiopathic(no known cause)
tonic/clonic seizures generally follow a pattern, however can skip steps:
- Aura - a sensation experienced by the pt before a convulsion occurs, eg. funny taste in mouth.
- Loss of consciousness.
- Tonic phase - body-wide rigidity.
- Hypertonic phase - arched back and rigidity.
- Clonic phase - rhythmic contraction of major muscle groups Arm, leg, head movement, lip smacking, biting, teeth clenching.
- Post-convulsion - major muscles relax, nystagmus(rapid eye movement) may still be occurring, eyes may be ‘rolled back’.
- Postictal - brain reseting. Can take minutes to hours before pt gradually returns to preconvulsion level of consciousness. during this time pt may be unable to speak(aphasic), confused, unable to follow commands, tired/sleeping. Gradually brain function will return to normal.
during a convulsion respirations may become very erratic, loud and obviously abnormal, or the pt may stop breathing and become cyanotic. these periods of apnoea are usually short lived and do not require assistance.
in contrast to tonic/clonic convulsions absences present with little movement. typically a child. child may simply stop moving, stop speaking mid sentence, rarely do they fall. usually only lasting seconds, no postictal period, no confusion, can be triggered by flashing lights or hyperventilation.
