7. stroke Flashcards
a patient walks with a wide unsteady gate and appears uncoordinated. Their speech is slurred. Where is the likely lesion?
cerebellum
42 year old suffers from a violent headache followed by sudden collapse. You notice that her left pupil is fixed and dilated and her left eye is deviated laterally and downwards. Which artery is most likely to have been affected?
posterior communicating artery - most likely to rupture - subarachnoid haemorrhage - ipsilateral 3rd nerve palsy
53 year old hypertensive man with sudden collapse; unable to move any part of his body except for eye movements, he appears to understand your questions, but is unable to answer. where is the likely lesion?
brain stem - ‘locked-in syndrome’
an elderly patient with a stiff flexed arm, and a stiff extended leg (both on the left) which the patient finds difficult to bend. Where is the cause most likely to be located?
upper motor neurone
a 30 year old pregnant lady complains to the GP of progressive hand weakness. She is unable to open jars ect. the GP noticed that the muscles around her thumb were wasting. Where is the most likely cause?
peripheral nerve - carpal tunnel syndrome
what are motor neurons
• Nerve cells responsible for relaying messages between the brain, central nervous system and peripheral nervous system
two neuron circuit
An upper motor neuron will synapse onto a lower motor neuron which will synapse onto a muscle
upper motor neurons
- Arise from the precentral gyrus and terminate in the ventral horn of the spinal cord
- UMN of the corticospinal tract leave the motor cortex and descend to the brainstem, entering the midbrain in large fibre bundles called the cerebral peduncles
- The tract continues down into the medulla where the fibres form two bundles, known as the pyramids
- At the base of the pyramids, about 90% of the fibres in the corticospinal tract decussate, or cross to the other side of the brainstem in a bundle called the pyramidal decussation
- The decussating fibres will then enter the spinal cord on the opposite side of the body from where they originated as part of the lateral corticospinal tract
- This tract will then synapse directly onto the lower motor neuron in the anterior horn of the spinal cord
- *The other 10% of the fibres will continue into the spinal cord on the same side of the body to then decussate at the spinal level – to synapse onto a lower motor neuron
UMN syndrome
- Damage anywhere to the descending tract before the anterior horn of the spinal cord
- Spastic paralysis – muscle is in spasm
- Hypertonic – hyper tone to the muscle because it is in spasm
- Hyperreflexia – knee reflex would be very rapid
- Disuse atrophy – wouldn’t be able to use the muscle overtime therefore atrophy
- Babinski -> tickle the bottom of the foot and the toes curl up towards the knee – an abnormal finding and a positive Babinski response
lower motor neurons
- Receive impulses from the upper motor neurons and connect the spinal cord and brain stem to the muscle fibres
- Cell bodies of the lower motor neurons are located in the grey matter of the spinal cord and brainstem
somatic reflex arc
- When muscle signals detect a sudden stretch -> the signal travels down the afferent nerve fibres
- Synapse on to the alpha motor neuron (monosynaptic reflex arc)
- The lower motor neuron innervates the effector muscle allowing for a quick muscle response
- A reflex arc allows for interpretation of and reaction on the stimulus immediately through the spinal cord -> bypassing the brain -> resulting in faster effector response.
LMN syndrome
• Lesions anywhere from the anterior horn of the spinal cord, peripheral nerve neuromuscular junction or muscle
• Flaccid – muscle is limp and not reacting
• Hypotonic – not in spasm / relaxed
• Hyporeflexia – knee reflex would not show any response
• Denervation atrophy – early atrophy due to no early spasm
- Babinski (normal – tickles the bottom on the foot and the toes should curl in / down towards the bottom of the foot – present in LMN lesion)
myasthenia Gravis
auto-immune disorder that affects the skeletal muscles
wake up feeling fine, end the day feeling weak
diplopia
Ptosis
• causes decreased ACh receptor function → worsens with muscle use
• B cells produce antibodies against post-synaptic nicotinic Ach receptors at the NMJ or proteins that are associated with the receptors
• Antibodies also attack proteins inside the muscle cells instead of the nicotinic ACh receptors → decrease in ACh receptor function
• ACh cannot bind → normal action potential cannot be initiated and propagated
• MG also causes an inflammatory response which leads to the destruction of ACh receptors
muscle disorders
- Inherited, progressive disorders caused by mutations in the gene that codes for Dystrophin
- Dystrophin links intracellular actin to the extracellular matrix to help stabilise the sarcolemma
- Genetic defect → mutated dystrophin protein → weaker sarcolemma → creatine kinase escapes and calcium enters the damaged cell → cell death → muscle degeneration → progressive weakness
Duchenne muscular dystrophy
• X-linked recessive inherited disorder
• Caused by a frameshift mutation (insertion or deletion of a nucleotide causing a change in the length of the polypeptide chain)
- so the dystrophin gene isn’t made and therefore dystrophin is not produced.
• Characterised by proximal-limb muscle weakness before distal limb muscle weakness, walking begins later in childhood, difficulty jumping/walking up steps, waddling gait, decreased mobility
