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Stroke and MCA- taken from Chinyee’s 2009 Neuroanat Essays
BLOOD SUPPLY OF BRAIN & STROKE (CEREBROVASCULAR ACCIDENT) Course & distribution of the MCA./ Name the structures (functional areas of cortex) supplied by the middle cerebral artery. The ICA enters the base of the skull and divides into the anterior & middle cerebral arteries (ACA,MCA). The MCA is the main continuation of the ICA (60 – 80% of ICA blood flow). MCA runs deep in the lateral fissure and sends terminal branches to the lateral surface of the frontal, parietal and temporal lobes (motor, sensory, auditory cortices) and the insula (a limbic related cortex). The MCA reaches the lateral surface of the hemispheres through the lateral sulcus. From the lateral sulcus, branches of the MCA spread across the lateral aspect of the frontal, parietal & temporal lobes. These branches do not extend to the margins of the lobes, and a definite watershed describes an arc around the lateral surface of the hemisphere. Branches & Structures they supply: 1. Cortical Branches • Superior (anterior) division - Frontal lobe − Post‐central gyrus (frontal parts) − Pre‐frontal cortex (involved in planning and interactions) − Lateral surface of motor & sensory homunculi − Expressive (Broca’s) area of dominant hemisphere (frontal lobe motor speech area) • Inferior (posterior) division - Parietal lobe, Temporal lobes − Optic radiations − Region of visual cortex related to macular vision − Receptive language (Wernicke’s) area of dominant hemisphere − Somesthetic association area (area 5) o Receives input from 1° somatosensory cortex o Indiv cortical modules have peripheral receptive fields covering several body segments o Multimodal - responds to both cutaneous & proprioceptive stimuli o Basis for stereognosis − Inferior parietal lobule (area 40) o Body schema = awareness of the existence & spatial relationships of body parts based on previous & current sensory experience o Receives visual & tactile info from the supplementary visual & somesthetic cortices 2. Deep Branches (penetrates to supply deep structures) • Lenticulostriate arteries (arise from the most proximal portion of the MCA) − Posterior limb of internal capsule (contains fibres running from thalamus to cortex, from cortex to thalamus/brainstem/spinal cord) − Part of basal nuclei (basal ganglia + hypothalamus) − Motor fibres (pyramidal tract) related to the face, hand, arm and leg as they descend in the genu and posterior limb of the internal capsule
2. and their excitatory neurotransmitters are released to the environment. Ischemic penumbra .g. Core ischemic zone Neurons in the core ischemic zone die due to ischemia. in stroke).What is ‘ischemic penumbra’? Within the ischemic cerebrovascular bed (e. there are two major zones of injury: 1.
hemiparesis.UMN will have loss of abdominal reflexes. Also risk of aspiration pneumonia increases.dressing. This is because the facial nucleus receives a bilateral supply from both cortices to supply the upper part of the face (the occipitofrontalis and the orbicularis oculi). whereas LMN will have abdominal reflexes. and also hyperreflexia.there is likely to be a dysarthria as well.Ambulation. The patient might also experience some problems with swallowing (dysphagia) and might need nasogastric feeding. . Food might need to be ground up. the lesion is likely to be affecting the left side of the brain. 45) is affected. if lesion was right sided. 3c)For muscles of the upper limb.this is an expressive aphasia. whereas LMN has flaccidity Clonus. further compromising on the patient’s ability to be understood.LMN will have. UMN won’t have In addition. leading to “telegraphic speech” and some degree of aphasia. hygiene.Swallowing. swallowing: . since it is a left sided lesion. As such.as above. It is also likely that Broca’s area in the left frontal lobe (area 44.UMN may have slight atrophy of disuse.difficult to bathe himself.speech is slurred because of the spasticity of the vocal muscles. 3a) see Chinyee’s notes above. eating. If lesion was rightsided. there could also be a left sided hemineglect. Because of the hemiparesis (and UMN lesion to the face area of the cortex). This only kills neurons with their cell bodies exposed to the excitatory neurotransmitters but spares those whose axons only have been dosed (because there are no glutamate receptors along axons). In this case. upgoing plantars (babinski’s). So looking at the problem in another way. hemiparesis. again.Hygiene. left sided hemineglect. Might need a walking stick (don’t prescribe a walking frame. 3b)The weakness is on the right side of the body (right-sided hemiparesis). hemiparesis. hence affected. and affecting the posterior division. further releasing excitatory neurotransmitters. ambulation. toileting. May have incontinence . LMN no clonus Weakness.motor problems.again.might not clean the left side . no babinski’s and areflexia Fibrillations/Fasciculations. difficulty in going to the toilet. whereas an UMN lesion will result in paralysis of the face contralateral to the site of the lesion (assuming lesion is above the medullary decussation of the corticoBULBAR tract).dysphagia . neurons still viable) The neurons here get overexcited and die. a LMN lesion will result in paralysis of the whole face on the ipsilateral side to the lesion.again. and face UMN vs LMN Tone.(area surrounding ischemic core. it affects the primary motor and sensory cortexleading to the right sided hemiparesis and hemihypesthesia (hemisensory deficit).Dressing.both have weakness Atrophy. for the face.UMN has spasticity (clasp-knife).spasticity of pharyngeal muscles.Toileting. that needs strength in both hands) .Eating. worsening the problem . LMN will have marked atrophy Reflexes. Likely to be an occlusion of the left middle cerebral artery (MCA). propagating the neuronal injury (excitotoxicity).UMN has clonus. in the case of the bADLsDEATHS. so this is spared.
The fibres then run to the lateral geniculate nuclei. and berry aneurysms increase the chance of hemorrhagic stroke. lesions lead to akinetopsia. Some are shared. oral contraceptives?) might increase chance of ischemic stroke. some fibres are given off to the pretectal nuclei. and colors. whereas the fibres from the temporal hemiretinas do not decussate.Chronic disease. as well as dual blood supply. At the optic chiasma. prosopagnosia. and the fibres from the nasal hemiretina of the right eye.probably the optic radiation.both ischemic and hemorrhagic stroke are possibilities. fibres from the nasal hemiretinas decussate. 4c) To give meaning to what we see. warfarin.as such.this is due both to the representation of the macula on both cortices. there may be some degree of macular sparing. also predisposes to plaque formation). especially hypertension and diabetes (in which the hyaline arteriolosclerosis affects the vascular walls and makes them leaky. so lesions can lead to agnosia.Drugs. V5. or anti-platelets like aspirin might increase chance of hemorrhagic strokes. and vice versa. hemangiomas. .Inherited conditions. 4a) The visual pathway from the retina to the visual cortex. like infective endocarditis or prosthetic valves. The fusiform gyrus is involved in recogising faceslesions in this lead to prospagnosia (fusiform gyrus impt for recognising forms. faces. or mural thrombus also increase the chance of ischemic strokes . 3a)The cerebellum’s role is to maintain balance and posture. 1rimary visual cortex would be affected on the left side.the vestibulocerebellum. Eg. signals pass in the optic nerve to the optic chiasma. whereas conditions resulting in coagulopathies (eg. Hence. There are 3 parts to the cerebellum.important in perceiving movement.3d) Risk factors for stroke: It depends on whether you are talking about an ischemic or a hemorrhagic stroke. or achromatopsia). leading to a right-sided homonymous hemianopia.From the retina. Arteriovenous malformations. running in the left optic tract would be fibres from the temporal hemiretina of the left eye. Anti-coagulants like heparin. which are responsible for the papillary reflexes. If occurs in the visual cortex. Basically: . The vestibulocerebellum is connected to the vestibular nuclei and . Valve problems. the spinocerebellum and the neocerebellum. The fibres then run in the optic radiation to the visual cortex (primary visual cortex in the calcarine sulcus of the occipital lobe) 4b) Visual field deficits.
If there is a unilateral lesion of the cerebellum. it is important in the coordination and planning of fine motor movements. Vestibulocerebellum (Archicerebellum). In the case of the spinocerebellum. often with nystagmus. intention tremor. . abduction.truncal ataxia. and rebound phenomenon (loss of interaction between agonist and antagonist smooth muscles) are also typical. Inputs from the cerebrum 1st go through the pontine nucleus (they don’t go straight to the cerebellum). in contrast to performance in posterior column disease.receives corticopontine inputs.so lesions result in gait ataxia (eg.gait ataxia.decomposition of movement Lesions of the vermis (midline). so that their attempts to touch an object will overshoot the target. and output goes back to the cerebral cortex.Loss of equilibrium.it will usually end at the lateral hemisphere of the cerebellum. in which people are unable to estimate the distance involved in muscular acts. tectospinal tracts Cerebrocerebellum. Decomposition of movement occurs.act on the rubrospinal. it is important for maintaining gait.is important for maintaining balance. Lesions in each of the three subdivisions of the cerebellum exhibit characteristic signs. Lesions of the neocerebellum-loss of coordination of voluntary movements 2001 Pros . where performance is adequate when the eyes are open .explosive speech .receive sensory inputs from trigeminal and spinalproprioception from the spinocerebellar tract. intention tremor. voluntary muscular movements become a series of jerky. decomposition of movements. also will have some amnesia and “cerebellar speech”.mainly related to flocconodular lobe and vermis of the cerebellum. also coordination of eye movements.Finger-to-nose and heel-to-knee test are performed w equal clumsiness whether eyes are opened or closed. Impt for planning and coordination of fine movement Disorders caused by cerebellar lesions are characterized by reduced muscle tone and a loss of coordination of smooth movements (see Table 13–2). unsteady gait). inability to toe the line even with eyes open. Impt for balance and eye movements Spinocerebellum. due to malfunction of the lateral vestibulospinal tract Spinocerebellum (Paleocerebellum) Truncal ataxia and "drunken" gait are characteristic. Neocerebellum Ataxia of extremities and asynergy (loss of coordination) are prominent. Dysmetria (past-pointing phenomenon) is also seen.paravermis zone.lesions in the vestibulocerebellum result in truncal ataxia and the tendency to fall towards the side of the lesion. In the case of the neocerebellum.so nystagmus (gaze dependent nystagmus). rebound phenomenon). Tend to fall towards the site of the lesion.And normal smooth trajectory of reaching movements replaced by stepped flexions. discrete motions rather than one smooth motion. dysdiadochokinesia. Dysdiadochokinesia (the inability to perform rapidly alternating movements). is typical. these abnormalities present on the same side as the lesion. Afferents go to the intermediate zone.so lesions result in dysmetria.Also remember “cerebellar speech”. Lesions of the anterior lobe. Impt for posture and motor execution.explosive speech 3b) skipped 3c) it is the left cerebellum that is affected Vestibulocerebellum.
in the left frontal lobe. and generalised lesions lead to anomic aphasia.the primary motor area. probably involving the upper limb area and maybe some part of the face as well. slurred speech). 45. area 44. Most lesions that involve Broca's area also involve the neighboring motor cortex. Note that it is unlikely to be a Wernicke’s aphasia. lesioning of Wernicke’s area leads to fluent aphasia.lesions result in aprosodias. hands is located closer to the lateral sulcus. Patients are often hemiplegic. Broca's aphasia often occurs as a result of strokes. as clearly he can understand verbal commands and ideomotor apraxia is unlikely.relates to which cerebral hemisphere is dominant. 3b) Motor speech area. Not so impt to know the blood supply. The lesion also extends to the primary motor cortex.there is the somatotopic arrangement along the precentral gyrus.located in the Broca’s area. but more importantly to know the area of defects.located in the Wernicke’s area. and the supplementary motor area.lesioning leads to receptive aphasia. and also inability to grasp sarcasm. rhythm of speech (prosody). the area for the legs is located closer to the midline between the hemispheres. 3c) In this example. most commonly affecting the middle cerebral artery territory. lesioning of the arcuate fasciculus connecting the Broca’s and Wernicke’s areas leads to problems with repetition.3a) Functional localisation of motor areas. with the arm more affected than the leg. The equivalent of the Broca’s and Wernicke’s areas in the right hemisphere is essential for understanding the emotional nuances and tone.thus leading to not just aphasia. mouth. etc. Sensory speech area. in the left frontal lobe. but is acutely aware of his problem “telegraphic speech”. Handedness. Lesioning of Broca’s area results in non-fluent aphasia. usually it is the left hemisphere. but also dysarthria due to psuedobulbar palsy (so thick. leading to Broca’s aphasiahence he has non-fluent aphasia. There is also the premotor area.lesioning leads to expressive aphasia. area 22. The lesion is probably involving the Broca’s area. . The area for the face. likely to be the middle cerebral @ that is lesioned.
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