Week 29 Aced! Presenting Symptoms Presenting Signs + Symptoms of CVA Stroke Syndromes According to Vascular Territory ACA: MCA Superior division:

Size: px

Start display at page:

Download "Week 29 Aced! Presenting Symptoms Presenting Signs + Symptoms of CVA Stroke Syndromes According to Vascular Territory ACA: MCA Superior division:"

Baldwin Watkins
5 years ago
Views:

1 Week 29 Aced! Presenting Symptoms M, 74 Fall Diabetes Overweight BP: 190/110 Smoker: ~60 pack/years Conscious Slurred Speech dysphasia (R) facial droop + (R) tongue deviation CN VII and XII Pupils + eye movement responsive CN II, III, IV, VI intact Sensation present in both limbs not sensory Power reduced in R limb (UL: 0/5 ; LL:2/5) Tricep (R:0; L:1) and Ankle (R:1;L:1) reflex reduced (R) Babinski response positive Mild Dysphagia Examination CT Scan CT shows a hypodense lesion in the left temporo- parietal region HYPODENSE due to H2O content the result of liquefactive necrosis Auscultation Registrar detects a left carotid bruit and commences anti- platelet therapy Thrombolytics (e.g. tpa or streptokinase) should only be used within a 3- HOUR WINDOW, and only if the patient fulfils a set of CRITERIA Neurological Difficulty swallowing and continuing problems with speech expressive dysphagia suggests damage to broca s area Patient coughs when drinking Statistics of Stroke 48,000 Australians are affected each year Third most common cause of death and most common cause of disability Haemorrhagic stroke has higher morbidity and mortality 2/3 of strokes occur in people > 65 years old Around 10% will have another stroke within the first 12 months Around 25% will have another stroke within 5 years Depression is very common following stroke (~2/3) ~20% of stroke patients die in hospital Presenting Signs + Symptoms of CVA Stroke Syndromes According to Vascular Territory ACA: contralateral paresis and sensory loss, loss of bladder control (hypertonic detrusor) MCA (proximal occlusion): Superior division: contralateral face and arm paresis and sensory loss, Broca s (expressive) aphasia (if in dominant hemisphere) Inferior division: contralateral homonymous hemianopsia (esp. inferiorly), contralateral agraphesthesia and asterognosis, anosognosia, contralateral neglect, Wernicke s (receptive aphasia) Internal carotid: premonitory TIA or transient monocular blindness (amaerosis fugax), asymptomatic or similar to MCA occlusion Basilar : Proximal (usually thrombosis): CN VI occlusion, impaired horizontal EOM, vertical nystagmus, reactive myosis, hemi- or quadriplegia Distal (usually embolic): decreased LOC, CN III palsy, decerebrate or decorticate posturing Posterior Inferior Cerebral Artery: ipsilateral ataxia, ipsilateral Horner s, ipsilateral facial sensory loss, contralateral impairment of pain and temperature, nystagmus, vertigo, dysphagia, dysarthria, hiccup Lacunar Infarcts (basal ganglia, thalamus, posterior limb internal capsule): Pure motor hemiparesis: contralateral arm, leg, and face Pure sensory loss: hemisensory loss (usually thalamic) Ataxic hemiparesis: ipsilateral ataxia and leg paresis Dysarthria- clumsy hand syndrome: dysarthria, facial weakness, dysphagia, mild hand weakness & clumsiness Risk Factors Fixed: Age Gender (male > female) Race Heridity Previous vascular event e.g. MI, stroke or PE High fibrinogen Modifiable: High BP Heart disease (AF, HF, endocarditis) Diabetes Hyperlipidaemia Smoking Excess alcohol consumption Polycythaemia OCP Social deprivation Types of Stroke 1. Ischaemic stroke (~85%) - occlusion of a blood vessel to the brain, generally due to embolus / thrombus 2. Haemorrhagic stroke (~15%) - ruptured vessel in brain tissue or subarachnoid space Subarachnoid haemorrhage intracranial bleeding in the subarachnoid space Due to aneurysm, trauma, rupture of an arteriovenous malformation, conversion of ischaemic stroke Intracerebral haemorrhage haemorrhage in the brain parenchyma, which may expand into the ventricles or subarachnoid space Due to hypertension, amyloid angiopathy, coagulopathy, AVM rupture, recreational drug use, trauma

2 Clinical Features Ischaemic Stroke Onset of signs/symptoms may be insidious or appear suddenly without warning Disruption of blood supply leads to functional disruption of the part of the brain being supplied Anterior cerebral Middle cerebral Posterior cerebral Vertebral/basilar arteries Poor judgement Altered mental status Contralateral hemiplegia/hemiparesis Urinary incontinence Gait apraxia Contralateral hemiplegia/hemiparesis Homonymous hemianopia Gaze preference towards affected side Aphasia (dominant hemisphere) Memory impairment Altered mental status Homonymous hemianopia Vertigo Nystagmus Double vision Dysphagia Progressive hemiparesis Uncoordinated/imprecise speech Facial hypesthesia Ataxia Progressive decline in consciousness Ipsilateral cranial effects Haemorrhagic Stroke Usually associated with altered consciousness or coma as well as headache, nausea and vomiting More likely to have seizures in haemorrhagic stroke Subarachnoid haemorrhage Abrupt onset of headache Progressive mental decline More diffuse neurological deficits than ischaemic stroke blood flows freely Intracranial haemorrhage Severe headache, nausea, vomiting Expanding haematoma Worsening oedema Decreasing consciousness (compression of brainstem) Disorders of Speech and Language: Broca s aphasia (expressive aphasia) Disorder of speech fluency laboured & short, lacks normal intonation + grammatically simple Relevant neuroanatomy: Broca s area posterior inferior frontal gyrus, dominant hemisphere = superior division, MCA Mechanism: lesion in Broca s area, larger lesions may affect the motor and sensory resulting in contralateral motor and sensory findings Wernicke s aphasia (receptive aphasia) Disorder of language comprehension speech is meaningless or strange, may contain paraphrasic errors Relevant neuroanatomy: Wernicke s area posterior superior temporal gyrus, dominant hemisphere = inferior division, MCA Mechanism: Lesion of inferior division of MCA, larger lesions may affect motor +/- optic pathways resulting in contralateral motor and sensory findings + contralateral homonymous hemianopia Treatments Goals: o Prevent further tissue damage and functional loss o Prevent reoccurrence o Maximise rehabilitation Treat hypo/hyperglycaemia aggressively to prevent worsening of the condition Blood pressure not immediately treated unless it is very high (>220/120 mmhg) Do not give the patient anything by mouth until a swallow screen has been completed Ischaemic Stroke Thrombolytics tissue plasminogen activator (tpa) up to three hours after onset of stroke Contraindicated in the case of previous haemorrhagic stroke, seizure, tendency to bleed, recent major surgery, recent head injury, heart infection, use of warfarin Anticoagulants for ischaemic stroke (after CT has been used to exclude haemorrhagic stroke) Surgery removal of atheromas or clots (endarerectomy) Rehabilitation and lifestyle modification to reduce reaoccurence Haemorrhagic Stroke 1. Helping the blood to clot - vitamin K, transfusion of platelets, synthetic clotting factors 2. Mild sedatives to control agitation 3. Prophylactic prevention of vasospasm with calcium channel blockers 4. May need surgery to remove intracerebral haematoma Neurotransmitters 3 classes of neurotransmitters: Amino acids GABA, Glycine, Glutamate, Aspartate Amines NA, Adrenaline, Dopamine, Serotonin, Histamine Peptides Hypothalamic releasing hormones (TRH, LHRH), Pituitary peptides (ACTH, Beta endorphin, TSH, GH, ADH, oxytocin), peptides that act on brain (Substance P, VIP, Insulin, glucagon, BDNF, gastrin, CCK), Others (Ang II, Bradykinin, calcitonin)

PPH Rehabilitation The stroke rehabilitation team requires a multidisciplinary approach Physiotherapists help to restore range of motion and balance Speech pathologists focus on communication

3 PPH Rehabilitation The stroke rehabilitation team requires a multidisciplinary approach Physiotherapists help to restore range of motion and balance Speech pathologists focus on communication problems as well as swallowing problems Medical doctors prevention and treatment Nurses daily care activities Rehabilitation nurses exercise paralysed or weakened limbs, educate patient and family Psychologists deal with mental and emotional aspect of stroke Social workers handle social challenges direct patients and family to appropriate resources Family members emotional support, encouragement, assistance with new activities Occupational therapists teach the patient daily living skills and how to use aids such as walkers Urologists treat urinary incontinence or bladder disorders Effects of Hypoxia The brain can be sustained for 5-10 seconds without oxygen Two compensatory mechanisms for O2: cerebral blood flow glycolysis anaerobic metabolism (glucose lactate + 2ATP) But also Acetylcholine, glutamate and GABA as well as acidosis Severe hypoxia leads to: Loss of ATP glutamate leakage excitation of cells attempting to maintain membrane potential (influx of Na+/Ca2+) further ATP loss, cell swelling, free- radical generation, enzyme activation Brain Metabolism Mainly by glycolysis Glycolysis highly favoured over gluconeogenesis enzymes for irreversible steps (HK, PFK, PK) Low levels of glycolytic and TCA intermediates there is also very low stored glycogen Ketones are only used in extreme conditions Very aerobic High CO2 output and oxidative phosphorylation Low lactate formation The citric acid cycle is important ATP synthesis Neurotransmitter production - Glu, GABA, Asp, Ach The process of neuronal ischaemia and infarction. 1. Reduction of blood flow reduces supply of oxygen and hence ATP. H+ is produced by anaerobic metabolism of available glucose (lactic acidosis). 2. ATP dependent membrane ionic pumps fail (Na/K- ATPase), leading to changes in cell ion concentrations and influx of water cytotoxic oedema and membrane depolarisation, allowing calcium entry and releasing glutamate that binds to glutamate gated ion channels. 3. Calcium enters cells via glutamate- gated channels. Elevated intracellular calcium activates membrane phospholipases (plus caspase pathway) and protein kinases, destroying intracellular organelles and the cell membrane, with release of free radicals. Free fatty acid release activates pro- coagulant pathways which exacerbate local ischaemia. 4. Ca directly interacts with mitochondria, overloading them and leading to apoptotic cell signaling pathways. 5. Glial cells take up H+ produced during lactic acidosis, can no longer take up extracellular glutamate and also suffer cell death, leading to liquefactive necrosis of whole arterial territory. 6. During ischemia, the hydrolysis of ATP via AMP leads to an accumulation of hypoxanthine. Increased calcium oxidises the hypoxanthine ROS further damage to cell membranes Infarction Necrotic core surrounded by poorly perfused region known as penumbra Penumbra (area around infarct) undergoes anaerobic metabolism acidotic damage Penumbra also damaged when reperfusion commences

Oxygen +glucose Anaerobic metabolism 1 H + ATP 5 Free radicals Thromboxane Prostaglandins Free fatty acids Cerebral Cortex Premotor Suppl motor Primary motor Corticospinal tract Corticonuclear tract

fibres that connect the caudate nucleus lentiform nucleus Lower Motor Neuron Lesion Upper Motor Neuron Lesion Muscle Strength Weakness/paralysis Weakness/paralysis Muscle Tone /absent muscle tone

area Thalamus Poliomyelitis, motor neuron disease, spinal cord injury at segmental level, peripheral nerve dysfunction, muscle myotonias, myasthenia gravis, muscular dystrophies Primary motor

4 Oxygen +glucose Anaerobic metabolism 1 H + ATP 5 Free radicals Thromboxane Prostaglandins Free fatty acids Cerebral Cortex Premotor Suppl motor Primary motor Corticospinal tract Corticonuclear tract Spinal Cord Lower Motor Neuron Dorsal root ganglion Sensory receptors Muscle contraction Basal Ganglia Brainstem Glia Fe + H Internal Capsule 6 H + K + Glutamate uptake by glia ocess of neuronal ischaemia and infarction. Lipid peroxidases Proteases NO synthase Na AMPA Glutamate NMDA Oedema Water Na + 2 Na + /K + ATPase 2 Depolarisation Anterior Limb: Contains fibres connecting thalamus; frontal lobe pons, and fibres that connect the caudate nucleus lentiform nucleus Lower Motor Neuron Lesion Upper Motor Neuron Lesion Muscle Strength Weakness/paralysis Weakness/paralysis Muscle Tone /absent muscle tone muscle tone Reflex strength /absent reflex strength reflex strength + Babinski sign Wasting Rapid muscle wasting Muscle mass maintained Causes Functional Regions of the Brain Motor speech (Broca s) area Thalamus Poliomyelitis, motor neuron disease, spinal cord injury at segmental level, peripheral nerve dysfunction, muscle myotonias, myasthenia gravis, muscular dystrophies Primary motor Cerebellum Spinocerebellar tracts Stroke (contralateral symptoms), cord section Primary somatosensory Taste area Sensory speech (Wernicke s) area Genu = apex (points medially); corticobulbar fibres Posterior Limb: Anterior part contains MOTOR fibres (of the corticospinal tract) o FAL = face, arms, legs (order) Secondary visual area Posterior part contains SENSORY fibres (projecting up to the postcentral gyrus) o fal = face, arms, legs (order) Primary auditory area Secondary auditory area Primary visual area

5 Relevant Neurological Signs Babinski response Abnormal cutaneous reflex response of the foot associated with UMN lesion; UMN signs may coexist spasticity, weakness, hyperreflexia Upgoing plantar response Common conditions: cerebral infarction, cerebral haemorrhage, spinal cord injury Sens: 45%; Spec: 98%; +ve LR: 19.0 Facial muscle weakness (unilateral) Decreased prominence of facial creases, loss of forehead furrows, widening of palpebral fissures facial droop Common conditions: MCA territory cerebral infarction, cerebral infarction Mechanism (UMN): weakness limited to lower contralateral facial muscles, due to bilateral supranuclear innervation and bilateral upper facial cortical representation in motor Hyperreflexia Stretch reflexes more brisk than normal; UMN = contralateral hyperreflexia Common conditions: cerebral infarction, cerebral haemorrhage, lacunar infarction Mechanism: UMN lesion gamma motor neuron activity + inhibitory neuron activity = hyperexcitability of alpha motor neurons Associated findings: spasticity, weakness, pronator drift, Babinski sign Spasticity Increased resistance to passive movement due to abnormal increase in resting muscle tone 3 x features: resistance = velocity- dependent, flexor- extensor tone dissociation, weakness present Mechanism: UMN lesion gamma motor neuron activity + inhibitory neuron activity = hyperexcitability of alpha motor neurons; absent during hyperacute period following UMN injury Tongue Deviation Deviates toward side of lesion Mechanism: genioglossus innervated by ipsilateral hypoglossal nerve and moves the tongue medially and forward Condition: medial medullary syndrome infarction of anterior spinal territory results in lesions of pyramidal tract, medial lemniscus and hypoglossal nuclei and fascicles Hypotonia Decreased resistance to passive movement due to decreased resting muscle tone Common conditions: radiculopathy, peripheral neuropathy, cerebellar infarction, cerebellar haemorrhage, hyperacute spinal injury Mechanism: hyperacute UMN disorder Sensory loss Characterised by the affected modalities (e.g. pain, temperature, light, touch, vibration, proprioception) and anatomical distribution Light touch, vibration and proprioception = dorsal column- medial lemniscus pathway; medulla Pain and temperature = spinothalamic tract pathway; spinal level/ventral white commissure Mechanism: ant. limb, internal capsule pure contralateral hemisensory loss of the face, arm and leg

Stroke School for Internists Part 1

Stroke School for Internists Part 1 November 4, 2017 Dr. Albert Jin Dr. Gurpreet Jaswal Disclosures I receive a stipend for my role as Medical Director of the Stroke Network of SEO I have no commercial