Neurology Hollie Wilson
Objectives Anatomy Physiology: Functional centres of brain UMN lesion vs. LMN lesion Spinal cord Main tracts ascending and descending Nerve roots and peripheral nerves action potentials Pathology Quiz
Cortical Organisation
Broca s and Wernicke s areas speech and language Broca s : frontal lobe Expressive language Wernicke s : temporal lobe Receptive language
Blood supply to the brain Anterior cerebral circulation INTERNAL CAROTID ARTERY Posterior cerebral circulation 2 VERTEBRAL ARTERIES Redundancy Anastomotic connections facilitate collateral blood supply in the event of narrowing or obstruction of a vessel
Three main pairs of arteries arising from circle of Willis ACA MCA PCA
Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery Medial brain Lateral brain Lateral and Medial Frontal lobe (primary motor cortex) Frontal lobe Occipital lobe (primary visual cortex) (Broca s, primary motor cortex) Parietal lobe (primary somatosensory cortex) Parietal lobe (primary somatosensory cortex) Superolateral temporal lobe (Wernicke s area) Inferior temporal lobe
Past question 1. Area of brain controlling speech? Broca s area 2. Location? Frontal lobe of dominant hemisphere 3. Blood supply? MCA
Past question Distinguish between dysarthria and dysphasia? Dysarthria is a speech disorder caused by disturbance of muscular control ie a problem with articulation Dysphasia/Aphasia is an impairment of language and may be receptive or expressive. Expressive (Broca s area) Receptive (Wernicke s area)
Stroke Aetiology Ischaemic (85%) Thrombosis Embolism Hypoperfusion Haemorrhagic (15%)
Risk factors Modifiable Hypertension DM AF Smoking Hyperlipidaemia Non modifiable Previous stroke/tia Increasing age FH ABCD2 score predicts risk of stroke following TIA
Clinical presentation Clinical presentation according to vascular territory involved MCA most commonly affected vessel Contra lateral hemiparesis Homonymous hemianopia Dysphasia Clinical History Time of onset Ix Blood glucose CT Brain
Visual field defects A good working knowledge of the visual pathway is important to aid with the localisation of cerebral lesions from clinical findings alone. 1. Complete loss of vision L eye (optic nerve lesion) 2. Bitemporal hemianopia (optic chiasm lesion) 3. Right homonymous hemianopia (optic tract lesion) 4. Right homonymous superior quadrantanopia 5. Right homonymous inferior quadrantanopia 6. Right homonymous hemianopia with macular sparing
Upper motor neuron lesions vs. lower motor neuron lesions An upper motor neuron is a motor neuron, that has it s cell body in the cerebral cortex, and synapses with lower motor neurons in the anterior horn cell or cranial nerve nuclei
N.B. The increased tone and hyperreflexia does not develop immediately following the development of an UMN lesion, due to a phenomenon called Spinal Shock. Initially the tone and reflexes will be reduced in an upper motor neuron lesion.
Upper spares upper
Story so far
Spinal Cord Tracts Ascending FROM periphery TO brain Mainly sensory feedback Descending FROM brain TO periphery Mainly motor control The spinal cord tracts run in the white matter of the spinal cord
Descending Spinal Cord Tracts 1. Corticospinal Tract (Pyramidal Tract) Primary Motor Cortex Internal capsule Other descending tracts to be aware of: 2. Vestibulospinal tract 3. Tectospinal tract 4. Reticulospinal tract Pons & Midbrain Crosses over at base of medulla Anterior horn of spinal cord
Corticospinal Tract Originates in the motor cortex (cortico) and terminates in the anterior horn cells of the spinal cord Passes through the internal capsule, down through the pons and midbrain Crosses over at the base of the medulla and forms a pyramidal bulge on the anterior aspect of the medulla (hence pyramidal tract). From here, it descends in the lateral aspect of the corticospinal tract to the anterior horn of the spinal cord, where it synapses with motor neurons
Recap: Action Potentials Na + influx K + efflux
Action Potential 1 Initiation The intra cellular environment of the axon is normally negative with respect to the extra cellular environment (resting membrane potential~ 70mV). All or nothing response a stimulus must decrease this potential (in other words make the inside of the axon less negative) in order to breach the threshold potential. Once the threshold potential is breached this results in a voltage dependent rapid increase in membrane permeability to Na +. The resultant influx of Na + results in depolarisation which reverses the potential across the neuronal cell membrane (the inside is now transiently positive and the outside negative).
Action Potential 2 Propagation Action potentials travel along an axon by saltatory conduction Gaps in the myelin sheath form nodes of Ranvier along the axon which allow the action potential to jump from node to node Conduction velocity is therefore increased by myelination and is also proportional to the axon diameter.
Action Potential 3 Repolarisation The same voltage dependent increase which facilitated Na + influx also facilitates a slower K + efflux K + efflux This loss of positive charge restores the normal negative resting membrane potential (repolarisation) Refractory period a second stimulus during this period will not result in depolarisation due to transient inactivation of Na + channels
Action Potential 4 Synaptic transmission Neurons are connected functionally by synapses between the axon of one neurone and the dendrites of another. Depolarisation of the pre synaptic membrane results in increased permeability to Ca 2+ by the opening of voltage gated Ca 2+ channels. Subsequent Ca 2+ influx causes fusion of synaptic vesicles with the presynaptic membrane and neurotransmitter release across the synaptic cleft. Binding of the neurotransmitter to receptor operated ion channels on the post synaptic membrane allows excitation or inhibition of the postsynaptic neurone.
The Neuromuscular Junction Terminal bouton of nerve fibres sits in infolding of sarcolemma (muscle cell membrane) called a junctional fold The Acetycholine receptors found at the neuromuscular junction are nicotinic acetylcholine receptors
Neuromuscular Transmission 1. Action potential travels down the axon of the neuron innervating the muscle fibre, leading to the opening of Voltage Gated Calcium Channels 2. This leads to influx of Ca 2+ 3. By an unknown mechanism, the increased Ca 2+ causes binding of vesicles containing acetylcholine to the pre synaptic membrane, causing release of acetylcholine into the synaptic cleft via a process called exocytosis 4. This acetylcholine binds to acetycholine receptors on transmitter gated ion channels, that open in response to the binding of acetylcholine 5. This causes Na+ influx into the muscle fibre 6. This deplolarises the muscle fibre, leading to the generation of an action potential within the muscle. This is known as an excitatory post synaptic potential or EPSP 7. In a process know as excitation contraction coupling, the action potential spreads to the sarcoplasmic reticulum via T tubules, and the arrival of an action potential to the sarcoplasmic reticulum leads to Ca2+ release from the organelle. This Ca2+ binds to Troponin C, and this leads to a conformational change that means that tropomyosin moves away from its normal binding site on the actin filament, allowing the myosin heads to bind to the actin filament and cause muscular contraction
Spinal Cord Tracts Ascending FROM periphery TO brain Mainly sensory feedback Descending FROM brain TO periphery Mainly motor control The spinal cord tracts run in the white matter of the spinal cord
Ascending Spinal Cord Tracts 1. The Posterior Column: fine touch, vibration and proprioception. These tracts cross over in the medulla, before terminating in the thalamus. From here, neurons leave the thalamus to ascend into the parietal lobe (primary somatosensory cortex) 2. The Spinothalamic Tract: anterior (crude touch) and lateral (pain and temperature) These tracts cross over at the level of the spinal cord at which they enter through the dorsal horn. Ascend in the spinal cord to reach the thalamus, from where there are projections to the parietal lobe 3. The spinoreticular tracts 4. The spinocerebellar tracts (unconscious proprioception)
Ascending Spinal Cord Tracts Fine touch Vibration Proprioception Crude touch Pain Temperature
Question: A 21 year old man was involved in a street fight and brought to ED. He sustained a knife wound to the left side of his neck which damaged his spinal cord unilaterally. What sensory and motor impairment will he have following this injury?
Objectives Anatomy Physiology: Functional centres of brain UMN lesion vs. LMN lesion Spinal cord Main tracts ascending and descending Nerve roots and peripheral nerves action potentials Pathology: strokes, spinal cord damage Quiz
QUIZ
Additional notes
Spinal Reflex Arc
Muscle Spindle Muscle mechanoreceptors that detect stretching of muscle fibres Composed of intrafusal fibres that run in parallel to extrafusal fibres that form the muscle bulk Act to regulate muscle tone and mediate tendon reflexes Action Potentials
Muscle Stretch vs Muscle Tension Muscle stretch: change in length of a muscle (usually an increase in length). This is detected by the muscle spindle that lies within the muscle. Spindles also detect the rate that the length of the muscle is changing (dynamic information). Muscle tension: weight/force applied to the end of a muscle, and is detected by the Golgi Tendon Organ, that lies within the muscle tendon.
Golgi Tendon Organ Also involved in muscle proprioception, but instead of signalling changes in muscle length, they signal changes in muscle tension Unlike muscle spindles, the 1b afferent fibres synapse with interneurons in the spinal cord, that in turn synapse with alpha motor neurones, to inhibit them Act to mediate the force of muscle contraction i.e grasping a pint glass hard enough to stop it falling, but not so hard that the glass smashes
Golgi Tendon Reflex