Tutorial 5 Alterations in CNS & PNS Flashcards

1
Q

Define consciousness and state how it is assessed

A
  1. The term “consciousness” has different meanings e.g. self-awareness or a state of alertness. In the context of this unit, we will define consciousness, as described to what extent a person is alert and awake, aware of their surroundings and how responsive they are to stimuli.
  2. In clinical situations, consciousness can be assessed using the Glasgow Coma Scale. The GCS measures the patient’s responses in terms of how the patient opens their eyes, verbal responses, and motor responses.
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2
Q

Which part of the brain plays a key role in the control of consciousness?

A

Reticular activating system (RAS)

a. part of the brain stem
b. consists of nuclei and tracts
c. regulates wakefulness, arousal and sleep

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3
Q

Describe common causes of altered levels of consciousness

A
  1. Altered level of consciousness can occur as the result of intracranial or extracranial causes
  2. Intracranial causes:
    e. g. head injury, haemorrhage, increased intracranial pressure, degenerative conditions, space-occupying lesions, and vasospasm of cerebral vasculature
  3. Extracranial causes:
    e. g. hypoxia, HTN, pH imbalance, systematic infection, hypo/hyperglycaemia, hepatic or renal dysfunction, medications or toxins
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4
Q

State how many strokes occur each year in Australia and list the major risk factors for stroke

A
  1. approx. 40,000 - 48,000 strokes occur each year AU
  2. It causes 7-10% of all deaths in AU
  3. Major risk factors:
    e. g. HTN, diabetes mellitus, hyperlipidemia, smoking, increased age, family history, alcohol consumption and heart disease
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5
Q

State the clinical manifestation of stroke

A
  1. Depending on the location and severity of the stroke, the patient may have problems with their motor, speech, sensory, language and cognitive functions
  2. The diagnosis of the cause of the stroke needs to identify whether it is haemorrhage or ischaemic
  3. CT, MRI and National Institute of Health Stroke Scale may be used in the assessment of the patient
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6
Q

Discuss the difference between the three most clinically important CNS infections: meningitis, encephalitis, and brain abscesses

A
  1. Meningitis:
    It can be identified as an infection of the brain and spinal cord. The majority of these infections are caused by viruses or bacteria (e.g. streptococcus pneumoniae)
  2. Encephalitis:
    It is an infection of the brain parenchyma. May be caused by viruses like herpes simplex or herpes zoster virus
  3. Brain abscesses
    They are accumulations of infective purulent material within the brain or associated with the CNS membranes. Mainly caused streptococci but can be caused by staphylococci and parasites.
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7
Q

Explain the pathophysiology that causes the symptoms of Meningococcal disease.

A
  1. Symptoms include severe headache, stiff/painful neck, sensitivity to light, vomiting and convulsions
  2. After invading the body, N. meningitides causes meningitis and severe septicaemia in children and adults
  3. This leads to localised inflammatory responses which result in cerebral oedema, raised intracranial pressure, and vascular thrombosis
  4. Increased vascular permeability leads to hypotension which is compounded by a loss of vascular tone in the later stage of the illness
  5. Myocarditis and myocardial depression may contribute to poor tissue perfusion, which can also impact on brain function
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8
Q

Define what is meant by the term “neurodegenerative disorder” and outline the common pathophysiological process implicated in neuro-degeneration

A
  1. Neurodegenerative disorders are disorders that produce a progressive chronic deterioration of the CNS
  2. This leads to observable changes in the structure and function of the brain and spinal cord
  3. Examples of neurodegenerative disorders include Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, motor neuron disease and multiple sclerosis
  4. The pathophysiology processes underlying different neurodegenerative disorders have recently been found to have some similarities.
    It has been proposed that common processes include: oxidative stress, intracellular protein aggregation, and mitochondrial dysfunction. Other mechanisms, which may also play a role, neuroinflammation, excitotoxicity, and apoptosis
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9
Q

Describe the clinical manifestation of Parkinson’s disease

A
  1. The cardinal signs of Parkinson’s are:
    a. tremor at rest
    b. rigidity
    c. akinesia (absence of spontaneous movement) or bradykinesia (slow movement)
    d. postural instability
  2. Just remember the acronym of TRAP
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10
Q

How is Parkinson’s disease diagnosed and managed?

A
  1. Parkinson’s disease is difficult to diagnose as usual blood tests cannot be used to diagnose Parkinson’s:
    a. They can be used to rule out other causes of the symptoms the patient is experiencing
    b. Neuroimaging also cannot be used to diagnose Parkinson’s but can rule out other causes
    c. The diagnosis of Parkinson’s disease is made on the basis of clinical picture and neurological and physiological signs and symptoms
  2. Loss of neurons in the substantia nigra results in dopamine deficiency and a relative increase in acetylcholine
    (substantia nigra - a basal ganglion that involved in movement reflection
    dopamine - neurotransmitter, induce feeling of pleasant
    acetylcholine -chief neurotransmitter of parasympathetic nervous system)
  3. Management of a patient with Parkinson’s takes a team of health professionals to manage challenges associated with dysphagia, postural HTN and postural instability
  4. Medication can be used to manage symptoms;
    e. g. dopamine precursors reduce symptoms by stimulating dopamine receptors, which reduce rigidity and tremor
  5. The patient may suffer from depression or anxiety as a result of their disorder and therefore may require treatment with selective serotonin reuptake inhibitor antidepressants. Constipation may also require treatment.
    (serotonin - a compound/neurotransmitter which constricts blood vessel
    reuptake - the absorption of presynaptic nerve ending of a neurotransmitter that it has secreted)
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11
Q

Compare and contrast Huntington’s disease, multiple sclerosis and motor neuron disease

A
  1. Huntington’s disease:
    an autosomal dominant genetic disorder that results in loss of neurons in the basal ganglia causing a decrease in activity of the inhibitory neurotransmitter GABA
  2. Multiple sclerosis:
    an autoimmune disorder whereby immune cells destroy CNS myeline leading to plaque formation and causing impairment in motor, sensory and neurological function
  3. Motor neuron disease:
    associated with degeneration of upper and lower neurons. Axons of the affected nerve degenerate leading to muscle wasting which begins as weakness and progresses to fatal paralysis
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12
Q

Is dementia a normal part of ageing?

A
  1. No, any change in cognition in an elderly person should be investigated
  2. UTIs can cause delirium and confusion which may be misdiagnosed as dementia
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13
Q

Compare and contrast the pathophysiology of primary and secondary head injury

A
  1. Primary head injury:
    results immediately from trauma e.g. bleeding
  2. Secondary head injury:
    occurs from processes initiated by the trauma within days to weeks which is a leading cause of brain injury-related death.
    e.g. ischaemia, increased ICP, cerebral oedema
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14
Q

Outline what are the possible causes of seizures and describe the different types of seizure

A
  1. Causes: abnormal levels of glucose or sodium, brain infection, brain injury, drugs, drug withdrawal, epilepsy, fever, extremely HTN
  2. Primary generalised seizures:
    begin with widespread electrical discharges across both sides of the brain. May be hereditary.
    e.g.
    Generalised tonic-clonic seizures:
    characterised by stiffening and jerking movements
    Absence seizures:
    patients stare into space
3. Partial seizures:
begin with an electrical discharge in one part of the brain.
e.g.
Simple or complex partial seizures
Secondarily generalised seizures
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15
Q

Describe the term pain

A
  1. Complex phenomenon
  2. Involves integration of stimulations of nociceptors - bare sensory nerve endings and input from higher brain centres
    Emotions and activities do modify the pain experience
  3. Biopsychosocial phenomenon
  4. Protective mechanism
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16
Q

What is the difference between acute and chronic pain?

A
  1. Acute: rapid onset, well localised, responds to analgesics
  2. Chronic: slowly developing continuous or recurring pain, difficult to treat, is a “learned” response involving glutamate and NMDA receptors.
    May be associated with hyperalgesia
17
Q

Discuss the different types of pain

A
  1. Somatogenic:
    due to recognisable physical cause e.g. burns, fracture
  2. Psychogenic:
    no obvious physical cause, however, still real pain in terms of measurable electrical activity
  3. Somatic:
    well localised pain from skin, muscles or joints, responds well to simple analgesics
  4. Visceral:
    poorly localised from organs in thoracic and abdominal cavity
  5. Referred:
    visceral pain which is perceived as somatic pain in an area with the same innervation
    e.g. liver and gallbladder pain is referred to right shoulder
18
Q

Explain why neuropathic pain may develop in an amputee in the affected limb

A
  1. Usually occurs to patients who had pain in the limb prior to amputation
  2. Pain is attributed to nerve remodelling where the sodium channels are more easily activated or are leaky
  3. The thalamus and cortical structures are also likely to be involved and the perception of pain in the affected limb may be related to the changes in the brain and not the periphery.
  4. Changes in the spinal cord are also implicated where changes in the responsiveness of NMDA glutamate channels occur.
19
Q

Describe the transmission of pain impulses

A

Pain impulses travel along the fibre of two main types:
1. A delta fibre:
a myelinated fibre present in skin the muscous membranes for rapid impulse transmission

  1. C fibre:
    smaller unmyelinated fibres located in the skin and deep tissues for slower transmission of impulses
20
Q

Describe the ascending pain pathway

A
  1. Carrier pain impulses to the brain
  2. Spinothalamic tract
  3. Information is carried to:
    a. 1st - dorsal root ganglion
    b. 2nd - dorsal horn
    c. 3rd - thalamus neurons
  4. Pain fibres cross over at their level of entry to the spinal cord
21
Q

How might the body inhibit the ascending pain pathway?

A
  1. By descending/inhibitory pathway
  2. Descending fibres release inhibitory substances such as:
    serotonin & endogenous opioid (encephalins)
  3. Well established that distraction reduces pain
22
Q

Describe the pathogenesis and common complications of spinal cord injury

A
  1. Pathophysiology of SCI consists of a primary and secondary phase of injury
  2. In the primary phase, the injury to the spine directly exerts a force to the spinal cord disrupting axons, blood vessels, and cell membranes.
    Neurological deficits are presented immediately
  3. The secondary injury leads to tissue destruction and involves inflammation, oedema, vascular dysfunction, ischaemia, excitotoxicity, and delayed apoptotic cell death
  4. CNS neurons do not repair. PNS neurons are capable of repair but only if the injury is near the distal end of axon.
  5. Normal functions of spinal cord cells at and below the level of injury ceases.
  6. SCI may lead to:
    a. Pressure sores due to putting pressure on the skin in the same position for long amounts of time.
    b. Osteoporosis - no weight bearing activity
    c. Pneumonia - infection due to decreased cough reflex
    d. UTI - bacteria reside in the bladder due to insufficient emptying
    e. Spasticity - exaggerated normal reflexes as of the disconnection between the brain and muscles
23
Q

Why do you think Dave is sweating profusely and experiencing nausea?

A
  1. Dave is experiencing severe pain and a sympathetic stress response
  2. The byproducts of the damaged cell are also stimulating the CTZ (chemoreceptor trigger zone)
24
Q

What is the triceps reflex and how could it be assessed?

A
  1. Simple stretch reflex. Bend arm, tap triceps tendon. Arm shoulder straighten.
  2. Both biceps and triceps reflexes are elicited probably to ensure that weakened reflex is due to a spinal problem, not merely damage to right arm musculature.
25
Q

What is a positive Babinski sign and what is the significance of this finding?

A
  1. Fanning out of toes when foot is stroked

2. Indicates spinal cord malfunction in the adult

26
Q

Which results from the tests and observations are consistent with SCI?

A
  1. Positive Babinski sign
  2. Weakened stretch reflexes on R
  3. Reduced movement and sensation on R
  4. Decreased temp and pain discrimination on L
27
Q

What are the possible causes of the loss of sensation and movement on the right side of Dave’s body?

A
  1. Sensory information travelling via the spinothalamic tract from the left hand side of the body, wouldn’t be experienced by higher brain centres. While it does cross over at the level of entry to the spinal cord, the signal is interrupted by the injury to the right hand side of C7 on.
  2. Sensory function may be affected because of the damage to the dorsal column (another ascending pathway) on the R - this column crosses over high up in the brain, with some fibres not crossing at all.
  3. Movement: possible damage to descending lateral corticospinal tract
28
Q

Explain how both sensory and motor function could be affected on one side only

A
  1. Spinal cord is probably more damaged on the R than on the L hemisection
  2. Motor function is affected on the same side as the injury because of damage to the corticospinal tract (descending pathway from the brain) which has already crossed over in the medulla oblongata
  3. Sensory function may be affected because of damage to the dorsal column (another ascending pathway) on the R - this column crosses over high up in the brain, with some fibres not crossing at all