13: Nervous System I Pathologies Flashcards
(41 cards)
1
Q
Carpal Tunnel Syndrome
A
- The median nerve becomes compressed in carpal tunnel syndrome.
- The Carpal Tunnel is a narrow passageway in the anterior wrist that contains tendons and the median nerve.
- This median nerve carries sensory information to the hand and controls movements in the hand and fingers.
2
Q
Carpal Tunnel Syndrome: Causes
A
- Fluid retention: pregnancy.
- Overuse –vibrating tools, desk posture.
- Due to: RA, hypothyroidism, acromegaly.
- Trauma (swelling), tumour or fracture in wrist. Small carpal tunnel (congenital).
3
Q
Carpal Tunnel Syndrome: Signs and Symptoms
A
- Tingling, numbness orpain in the median nerve distribution.
- Symptoms are often worse at night and can wake patient.
- Weakness of grip and weak thumb opposition.
- Muscle wasting at base of the thumb (sensory symptoms 1st).
4
Q
Carpal Tunnel Syndrome: Diagnosis
A
- Tinel’s test & Phalen’s test (+ve if reproduces hand symptoms).
- Nerve conduction studies
5
Q
Carpal Tunnel Syndrome: Treatment
A
- Anti-inflammatory drugs, corticosteroid injection, splinting the wrist, physiotherapy.
- Surgery (cutting transverse carpal ligament).
6
Q
Carpal Tunnel Syndrome: Complications
A
• In chronic and / or untreated cases, the muscles at the base of the thumb may degenerate.
7
Q
Bell’s Palsy
A
The nerve that controls the facial muscles (facial nerve) becomes inflamed or compressed.
8
Q
Bell’s Palsy: Causes
A
Viral e.g. Herpes simplex
Surgery
Injury.
9
Q
Bell’s Palsy: Signs and Symptoms
A
- Sudden unilateral weakness or paralysis of the facial muscles.
- Cannot close affected eye (can damage cornea).
- Loss of taste & intolerance to loud noise if severe.
10
Q
Bell’s Palsy: Treatment
A
Acyclovir
Cortisone
11
Q
Guillain-Barre Syndrome
A
- Guillain-Barre is a form of post-infectious de-myelinating disease with ‘neuritis’.
- Associated with acute, ascending, progressive inflammation and demyelination of peripheral nerves.
12
Q
Guillain-Barre Syndrome: Causes
A
Auto-immune. 75% are triggered by a recent infection (1-3 weeks after respiratory/GIT infection or post-vaccination e.g. flu / EBV). Antibodies formed against virus cross react with lipids in myelin –molecular mimicry
13
Q
Guillain-Barre Syndrome: Signs and Symptoms
A
- Sudden, progressive, bilateral, ascending paralysis.
- Paraesthesia and sensory changes.
- Neuropathic pain into legs.
14
Q
Guillain-Barre Syndrome: Diagnosis
A
• Nerve conduction studies, lumbar puncture.
15
Q
Guillain-Barre Syndrome: Treatment
A
- Emergency care -respirator, intensive care.
* Plasma exchange, intravenous antibodies, corticosteroids.
16
Q
Guillain-Barre Syndrome: Complication
A
Death by heart or respiratory failure.
17
Q
Multiple Sclerosis (MS)
A
- An autoimmune inflammatory disease causing demyelination of axons in CNS neurons with damage.
- T lymphocytes attack myelin antigens. Multiple areas of sclerosis (scar tissue) along axons which disrupts conduction.
- Usually occurs between 20-50 years of age, affecting women (2:1) to men.
- Most MS follows a relapsing-remitting pattern(85%). Other patters are progressive.
18
Q
Multiple Sclerosis (MS): Prognosis
A
Depends on disease pattern. 15% only suffer one episode. Progressive types have a poor prognosis.
19
Q
Multiple Sclerosis (MS): Causes
A
- Vitamin D deficiency –higher prevalence further away from the equator.
* Vitamin D has been shown to ↑oligodendrocyte production of myelin. - Vitamin B12 deficiency –normally acts as a co-factor in myelin formation and also has immunomodulatory effects.
- Genetic susceptibility & environmental trigger, dietary risk factors. Slightly increased risk with family history.
- Viruses e.g. Epstein –Barr Virus (EBV), measles etc.
20
Q
Multiple Sclerosis (MS): Signs and Symptoms
A
- Visual symptoms are common: Blindness, loss of vision of one eye & occasional pain (neuritis). Double vision & nystagmus (jerking of eyeball).
- Deafness and loss of balance.
- Burning, pulling sensations.
- Tingling and loss of sensation.
- Bladder urgency and incontinence.
- Cognitive changes and depression.
- Weakness.
21
Q
Multiple Sclerosis (MS): Diagnosis
A
• No definite test: based on clinical findings, MRI ophthalmoscopy and CSF analysis.
22
Q
Multiple Sclerosis (MS): Treatment
A
Immunomodulatory therapies: Corticosteroids, Interferon-beta,
Physiotherapy
Symptom management
23
Q
Motor Neuron Disease (MND)
A
- MND describes the progressive degeneration of motor neurons in the spinal cord, motor cortex & brain stem.
- The current hypotheses focuses on abnormal mitochondrial function causing oxidative stress in motor neurons.
- Sensory functions remain intact.
- Age of onset is typically >40yrs (highest incidence 50-70yrs).
- More commonly affects men.
24
Q
Motor Neuron Disease (MND): Causes
A
• Unknown. Suspected link with genetics & environmental toxins and oxidative stress.
25
Motor Neuron Disease (MND): Signs and Symptoms
* Typically presents as weakness in upper limbs -> dropping objects or difficulty manipulating objects.
* Wasting of hand muscles & tremor of limbs at rest.
* Later stages can affect the legs (tripping), cause slurred speech, dyspnoea, difficulty swallowing.
* Death by respiratory failure -typically within 3-5yrs.
26
Motor Neuron Disease (MND): Treatment
Currently no cure, specialist care.
27
Dementia
* Dementia is a syndrome caused by a number of brain disorders, which cause:
* Memory loss.
* Decline in other aspects of cognition.
* Difficulty performing daily activities.
* The prevalence of dementia rises with age.
28
Dementia: Types
1. Alzheimer’s disease (50%) – degeneration of
the cerebral cortex and reduced Acetylcholine
production.
2. Vascular dementia (25%) - due to
cerebrovascular disease (e.g. due to stroke/s)
and poor oxygen delivery.
29
Alzheimer’s Disease
• Alzheimer’s is a neurodegenerative disease of the cerebral cortex.
• Associated pathologically with abnormal protein deposition (beta amyloid), atrophy of neurons and less acetylcholine.
• The hippocampus is among the areas first affected, which is important for memories.
The amygdala is often affected later and is a key centre for emotions & memories.
• Whilst progressing, additional regions of brain become affected.
• It is the most common type of dementia (50%)
• 20% of the population affected by 80 years of age.
• Brain deterioration is thought to begin decades before symptoms become evident.
• Global neuron atrophy (& hence brain shrinkage) with disrupted cell communication (Ach).
30
Alzheimer’s Disease: Causes
• Heavy metal toxicity (degenerate the blood brain
barrier):
•High copper & mercury.
•Aluminium toxicity(e.g. from vaccines, cans, foil etc.).
• Genetic links (account for <1%) – ApoE4 gene.
• Chronic inflammation:
•Such as sugar (& insulin resistance), dairy, gluten.
•Leaky gut (promoting inflammation).
• Pathogens (micro-organisms):
•Oral bacteria such as P.gingivalishave been identified in tissue biopsies.
•Herpes simplex virus.
• Increased risk if cardiovascular disease (CVD) & high homocysteine.
• High levels of oxidative stress.
• Higher cortisol levels (chronic stress).
• Nutritional deficiency e.g. B1, B3, B6, B12, folate, omega-3 fatty acids.
• Hormonal factors:
• Oestrogen deficiency (effects mostly seen in women following full hysterectomy) & Testosterone deficiency.
•Thyroid hormone deficiency.
31
Alzheimer’s Disease: Signs and Symptoms
Early stages:
• Slight memory loss (especially short term) i.e. forgetting recent conversations.
• Repeated questions & confusion.
• Decreased initiative (↓hobbies, ↓hygiene).
Later stages:
• Significant memory loss (incl. long-term memory).
• Subtle changes in higher order functions i.e. understand jokes.
• Mood disturbances: agitation & aggression.
• “Loss of sense of self” -autobiography (left hippocampus).
• Difficulty with language, unsteady, depression.
32
Alzheimer’s Disease: Investigations
* Mini Mental State Exam.
| * MRI & CT scan.
33
Alzheimer’s Disease: Treatment
* Drugs: Acetylcholinesterase inhibitors (ineffective).
| * Psychological treatments such as cognitive behavioural therapy (CBT).
34
Alzheimer’s Disease: Pronosis
• People typically live for anywhere between 5 and 20 years after the onset of Alzheimer’s symptoms. The most common cause of death is infection.
35
Parkinson’s Disease
* A progressive neurological movement disorder affecting movement.
* Caused by loss of dopaminergic neurons in the substantia nigra: an area of the midbrain that regulates movement (and reward).
* Affecting approx. 1% of individuals over 60.
36
Parkinson’s Disease: Causes
* Mitochondrial dysfunction (oxidative stress).
* Constipation & diet low in polyunsaturated fats. Genetics.
* Toxic environmental factors: i.e. carbon monoxide, manganese poisoning, exposure to pesticides & herbicides.
37
Parkinson’s Disease: Pathophysiology
2 major neuropathological findings in the medical model:
1. Degeneration of dopaminergic neurons in the substantia nigra (midbrain) causing dopamine deficiency leaving patients less able to direct or control their movement.
2. Accumulation of abnormal proteins (Lewy Bodies) within neurons.
38
Substantia nigra
“black substance” –has a darker appearance due to high levels of neuromelaninin dopaminergic neurons.
39
Parkinson’s Disease: Signs and Symptoms
* Bradykinesia: Short shuffling steps (difficulty stopping/starting).
* Resting tremor(“pill rolling”).
* Stopped/flexed posture.
* Lack of normal subconscious movements (swinging arms).
* Muscle rigidity, mask-like face, low voice.
40
Parkinson’s Disease: Treatment
* Dopamine replacement (Levodopa/L-dopa).
* Doesn’t cross blood brain barrier very well so high doses needed, side effects can lead to abnormal movements.
* Deep brain stimulation (electrodes in brain).
41
Huntington’s Disease
* Inherited neurodegenerative disorder affecting the basal ganglia.
* Results in loss of muscle co-ordination (abnormal involuntary jerky movements called ‘chorea’).
* Also causes cognitive impairment and loss of intellect.
* Poor regulation of mood and emotions: psychiatric symptoms (depression, aggression etc.)
* A genetic (autosomal dominant) disease with a defect on chromosome 4.
