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Neurology Motor control and movement disorders Trisha Choudhary Intercalating medical student from BSMS 9/11/2023 @ BRITISHINDIANMEDICASSOCIATION @BINDIANMEDICS BRITISH INDIAN MEDICAL @BIMA ASSOCIATION BIMA Preclinical series WHO AM I Your picture • Medical student from Brighton and Sussex Medical School rd th • Intercalating between 3 and 4 year • BSc Cardiovascular sciencesTOPICS COVERED 1.Motor control overview: • Motor cortex and descending pathways • Basal ganglia • Cerebellum 2.Movement disorders 3.SBAsMotor control – The basics Where is the motor cortex located in the Cerebrum? A. Frontal Lobe B. Occipital lobe C. Parietal lobe D. T emporal lobe E. Cerebellum The motor cortex Primary motor cortex Central sulcus Supplementary Function: •Control of Voluntary movement motor area Premotor cortex Frontal lobe Location: •Frontal lobe Further split •Primary motor cortex •Premotor cortex up into: •Supplementary motor cortex •Map of the different muscle areas Homunculus of the body in the primary motor Medial Lateral cortex Within the primary motor cortex Descending motor pathways •Motor signals transmitted Directly or Indirectly (multiple accessory pathways e.g. basal ganglia and cerebellum) •Pyramidal or ExtrapyramidalCorticospinal tract • 90% of fibers cross over in medulla – Lateral corticospinal tract • 10% fibers do not cross over – Anterior corticospinal tract • They cross over in the spinal cord Ventral horn Lateral columns Anterior columnsThe Basal ganglia Work in association with cerebral cortex enabling Function: execution of smooth movement Cerebral cortex Thalamus Basal ganglia • Pars Compacta • Pars reticulata What is the main excitatory Neurotransmitter? A.GABA B.Glutamate C.Dopamine D.Serotonin E.AcetylcholineIndirect and Direct pathways of the basal ganglia Neurotransmitters: Dopamine is released from Substantia nigra pars compacta GABA is inhibitory Glutamate is excitatory The cerebellum Anterior lobe Posterior lobe lobeculonodular Function: • Coordinate movements • Control posture, balance • Cerebellum can be split up anatomically into lobes and fine motor movement • Each lobe receives inputs from different areas of CNS forming different functional zones • Motor learning Spinocerebellar Receives inputs from the spinal cord Controls muscle tone/ posture particularly of the truncal muscles Receives inputs from the cerebral cortex Cerebrocerebellar Controls planning and movement initiation especially of fine movementsMovement disorders UMN Vs LMN lesions Upper motor Neuron Lower motor neuron Lesion Cerebral hemisphere – anywhere above Lesion below anterior horn cell to the relevant muscle anterior horn of spinal cord Tone Hypertonia Hypotonia Spasticity Flaccid Power Reduced Reduced Particularly in Upper limb extensors In distribution of affected motor root/ nerve and lower lib Flexors Reflexes Hyperreflexia (brisk) Hyporeflexia Babinski reflex Upgoing/ extensor Babinski Normal Muscle wasting Not predominantly Present Fasciculations Absent PresentUpper Motor Neuron Lesions •Stroke •Motor neuron disease •Amyotrophic lateral sclerosis Condition summary – Stroke PATHOPHYSIOLOGY INVESTIGATIONS Ischemic: Occlusion of blood vessel Non- contrast CT Head +/- CT angiogram (85%) ECG • Emboli • Thrombus Bloods – to check for risk factors (such as high cholesterol, diabetes) • Dissection Hemorrhagic: Bleeding (15%) MANAGEMENT Ischemic: conservative measures including stabilsing patient, antiplatelets, Thrombolysis (within < 4.5. hours of symptom onset and excluding hemorrhage) Hemorrhagic: STOP anticoagulation, seek neurosurgical advice PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • DVT due to immobility in recovery • Aspiration pneumonia – unable to swallow (dysphagia) 110,000 cases each year with • Weakness, impaired mobility and seizures (Neurological sequalae) • Depression a mortality of 11% • Prognosis depends on the type of stroke Condition summary – Motor neuron disease PATHOPHYSIOLOGY INVESTIGATIONS Neurodegenerative disorder affecting = both upper and • Majorly a clinical diagnosis – investigations rule out other pathology lower motor neurons • Electromyography Selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells • Nerve conduction studies MND never affects eye movements, senses or sphincters • MRI of spine – rule out spinal pathology (can mimic MND) Various different types: • Pulmonary function tests (risk of respiratory failure) • Amyotrophic lateral sclerosis (50%) • UMN – affects corticospinal tracts • LMN – also affects anterior horn cells • Presents with both UMN and LMN signs MANAGEMENT • Progressive bulbar palsy • Riluzole – ALS, protects motor neurons from glutamate damage • Affects cranial nerves (IX-XII) • Speech and swallowing issues • Respiratory support • Supportive treatment • Progressive muscular atrophy • LMN – anterior horn cells PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Short life span (3 years due to respiratory failure) • Depends on subtype for prognosis • Mostly in above 40 • ALS affects around 4-5 in 100,000 people • Old age, poor respiratory function are poor prognostic factors • Complications: Aspiration pneumonia, bronchopneumonia, respiratory failureLower motor neuron Lesions Anterior cord syndrome •Loss of motor function below level Brown-Sequard syndrome •Hemisection lesion of the spinal cord •Unilateral spastic paralysisWhich of the following clinical findings are typically associated with upper motor neuron (UMN) lesions, as opposed to lower motor neuron (LMN) lesions? A. Muscle atrophy and fasciculations B Hyperreflexia and spasticity C. Hyporeflexia and muscle weakness D. Flaccid paralysis and reduced muscle tone E. Normal Babinski reflex Basal ganglia movement disorders Hypokinetic: • Parkinson’s disease • Parkinsonism - Lewy body dementia, Vascular , Drugs (e.g. neuroleptics, metoclopramide) Hyperkinetc • Hemiballismus • Chorea • Huntington’s • Tics (ourette’s) Condition summary – Parkinson’s disease PATHOPHYSIOLOGY INVESTIGATIONS • Mostly a clinical diagnosis Neurodegenerative disorder • MRI brain (does not diagnose PD) • Loss of dopaminergic neurons In substantia • DaT scan (SPECT): single photon emission computed tomography – reduced dopamine uptake in basal ganglia nigra pars compacta • Aetiology is idiopathic (genetic involvement) • Histology - inclusion bodies (misfolded α- synuclein called Lewy bodies Parkinsonism: • Bradykinesia MANAGEMENT • Tremor • Rigidity • Postural instability L-dopa with decarboxylase inhibitor Other medications: • Dopamine agonists e.g.Ropinirole • Monoamine oxidase inhibitor e.g. Selegiline Non-pharmacological: • Deep brain stimulation (Subthalamic nuclei) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Chronic and progressive (no cure!) • Life expectancy is reduced • Mainly effects elderly (above 60 years) • Increased risk of dementia Hyperkinetic movement disorders Hemiballismus Tics Definition: Sudden flailing movements of an entire limb Definition: Brief, stereotyped repeated movements Pathophysiology – lesion in the subthalamus most commonly caused by Tourette’s syndrome is motor and vocal tics occur stroke Associated with co-morbid conditions https://www.youtube.com/watch?v=RAATfknm1F4 Chorea Definition: Jerk, brief irregular contractions (not repetitive or rhythmic) but flow rhythmically (dance like) Pathophysiology - Multiple small lesions in the putamen common cause – Huntington’s disease • Autosomal dominant – CAG repeat • Resulting in degeneration of cholinergic and GABAergic neurons • Due to defect in Huntington gene on chromosome 4 https://www.youtube.com/watch?v=RxWEilu-Mf4Cerebellar lesion – manifestations Dysdiadochokinesia Ataxia Nystagmus Intention tremor Slurred staccato speech HypotoniaSBAsQuestion 1 Which of the following is NOT a characteristic of Parkinson's disease? A. Bradykinesia B. Resting tremor C. Exces ive production of acetylcholine D. Rigidity E. Postural instability Question 2 A 52-year-old woman is referred to a neurology clinic as she has been experiencing jerky movements of her arms and legs that she finds difficult to control. The most likely diagnosis is Huntington's disease, which causes degeneration of the basal ganglia. What neurotransmitters will be predominantly affected to cause this woman's symptoms? A.Ach and GABAA B. ACh and Glutamate C. GABA and NA D. Glutamate and NA E. NA and AChQuestion 3 Which structure is a common target for deep brain stimulation in Parkinson’s disease? A. dentate nucleus B. Edinger-Westphal nucleus C. nucleus accumbens D. nucleus basalis of Meynert E. Subthalamic nucleussTHANK YOU FOR LISTENING ANY QUESTIONS INSERT QR CODE FOR FEEDBACK FORM BIMA Preclinical series