Neuroanat- Stroke- Visual Pathway, Cerebellum, and Speech Areas 1.

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

in stroke).What is ‘ischemic penumbra’? Within the ischemic cerebrovascular bed (e. and their excitatory neurotransmitters are released to the environment.g. there are two major zones of injury: 1. Core ischemic zone Neurons in the core ischemic zone die due to ischemia. 2. Ischemic penumbra .

Toileting.there is likely to be a dysarthria as well. hence affected. a LMN lesion will result in paralysis of the whole face on the ipsilateral side to the lesion. whereas LMN has flaccidity Clonus.Ambulation.Dressing. and also hyperreflexia. eating.(area surrounding ischemic core. If lesion was rightsided. Also risk of aspiration pneumonia increases. 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). left sided hemineglect.motor problems. worsening the problem .Swallowing. hemiparesis. and face UMN vs LMN Tone. LMN no clonus Weakness. 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).UMN has spasticity (clasp-knife). whereas LMN will have abdominal reflexes. further releasing excitatory neurotransmitters.might not clean the left side . since it is a left sided lesion. 3b)The weakness is on the right side of the body (right-sided hemiparesis). 3c)For muscles of the upper limb. again. 3a) see Chinyee’s notes above.LMN will have. Because of the hemiparesis (and UMN lesion to the face area of the cortex).again. . it affects the primary motor and sensory cortexleading to the right sided hemiparesis and hemihypesthesia (hemisensory deficit).speech is slurred because of the spasticity of the vocal muscles.UMN will have loss of abdominal reflexes. difficulty in going to the toilet. hygiene. the lesion is likely to be affecting the left side of the brain.Eating. and affecting the posterior division. Might need a walking stick (don’t prescribe a walking frame. swallowing: .UMN has clonus.dressing. The patient might also experience some problems with swallowing (dysphagia) and might need nasogastric feeding. so this is spared. hemiparesis. As such.Hygiene.difficult to bathe himself. In this case.as above. no babinski’s and areflexia Fibrillations/Fasciculations. neurons still viable) The neurons here get overexcited and die.again. So looking at the problem in another way. upgoing plantars (babinski’s). toileting. there could also be a left sided hemineglect. in the case of the bADLsDEATHS. propagating the neuronal injury (excitotoxicity). further compromising on the patient’s ability to be understood. leading to “telegraphic speech” and some degree of aphasia. Likely to be an occlusion of the left middle cerebral artery (MCA).dysphagia . for the face. 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). hemiparesis. if lesion was right sided. It is also likely that Broca’s area in the left frontal lobe (area 44. 45) is affected. May have incontinence .both have weakness Atrophy. ambulation. Food might need to be ground up. that needs strength in both hands) . LMN will have marked atrophy Reflexes.UMN may have slight atrophy of disuse.spasticity of pharyngeal muscles. UMN won’t have In addition.this is an expressive aphasia.

There are 3 parts to the cerebellum. and vice versa. also predisposes to plaque formation). If occurs in the visual cortex. there may be some degree of macular sparing.as such.Chronic disease. 4c) To give meaning to what we see. 3a)The cerebellum’s role is to maintain balance and posture. and the fibres from the nasal hemiretina of the right eye. The fusiform gyrus is involved in recogising faceslesions in this lead to prospagnosia (fusiform gyrus impt for recognising forms. 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. Arteriovenous malformations. or mural thrombus also increase the chance of ischemic strokes . as well as dual blood supply. whereas conditions resulting in coagulopathies (eg. The fibres then run to the lateral geniculate nuclei. especially hypertension and diabetes (in which the hyaline arteriolosclerosis affects the vascular walls and makes them leaky. and colors. Basically: . lesions lead to akinetopsia. whereas the fibres from the temporal hemiretinas do not decussate. oral contraceptives?) might increase chance of ischemic stroke. faces.this is due both to the representation of the macula on both cortices.both ischemic and hemorrhagic stroke are possibilities. . Eg. hemangiomas. Hence. prosopagnosia.the vestibulocerebellum.probably the optic radiation. fibres from the nasal hemiretinas decussate. Some are shared. signals pass in the optic nerve to the optic chiasma.Drugs. which are responsible for the papillary reflexes. At the optic chiasma. running in the left optic tract would be fibres from the temporal hemiretina of the left eye. leading to a right-sided homonymous hemianopia. 1rimary visual cortex would be affected on the left side. or achromatopsia). Valve problems. the spinocerebellum and the neocerebellum. or anti-platelets like aspirin might increase chance of hemorrhagic strokes. V5. The vestibulocerebellum is connected to the vestibular nuclei and . 4a) The visual pathway from the retina to the visual cortex.Inherited conditions.important in perceiving movement.3d) Risk factors for stroke: It depends on whether you are talking about an ischemic or a hemorrhagic stroke.From the retina. so lesions can lead to agnosia. and berry aneurysms increase the chance of hemorrhagic stroke. warfarin. like infective endocarditis or prosthetic valves. Anti-coagulants like heparin. some fibres are given off to the pretectal nuclei.

so that their attempts to touch an object will overshoot the target. is typical. dysdiadochokinesia. in which people are unable to estimate the distance involved in muscular acts. Dysmetria (past-pointing phenomenon) is also seen. 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). often with nystagmus. also coordination of eye movements. it is important for maintaining gait.truncal ataxia. and output goes back to the cerebral cortex. in contrast to performance in posterior column disease. and rebound phenomenon (loss of interaction between agonist and antagonist smooth muscles) are also typical.decomposition of movement Lesions of the vermis (midline). it is important in the coordination and planning of fine motor movements.explosive speech 3b) skipped 3c) it is the left cerebellum that is affected Vestibulocerebellum.And normal smooth trajectory of reaching movements replaced by stepped flexions. discrete motions rather than one smooth motion. Lesions of the neocerebellum-loss of coordination of voluntary movements 2001 Pros . where performance is adequate when the eyes are open . intention tremor. . Afferents go to the intermediate zone. these abnormalities present on the same side as the lesion.paravermis zone.Finger-to-nose and heel-to-knee test are performed w equal clumsiness whether eyes are opened or closed. In the case of the neocerebellum.is important for maintaining balance.gait ataxia. rebound phenomenon). inability to toe the line even with eyes open. If there is a unilateral lesion of the cerebellum.so nystagmus (gaze dependent nystagmus). voluntary muscular movements become a series of jerky. Impt for balance and eye movements Spinocerebellum.Also remember “cerebellar speech”. Impt for posture and motor execution. intention tremor. Decomposition of movement occurs.lesions in the vestibulocerebellum result in truncal ataxia and the tendency to fall towards the side of the lesion.receives corticopontine inputs.mainly related to flocconodular lobe and vermis of the cerebellum. Dysdiadochokinesia (the inability to perform rapidly alternating movements).Loss of equilibrium. Vestibulocerebellum (Archicerebellum).explosive speech . unsteady gait). tectospinal tracts Cerebrocerebellum. Lesions of the anterior lobe. Neocerebellum Ataxia of extremities and asynergy (loss of coordination) are prominent.so lesions result in gait ataxia (eg. due to malfunction of the lateral vestibulospinal tract Spinocerebellum (Paleocerebellum) Truncal ataxia and "drunken" gait are characteristic.act on the rubrospinal. Lesions in each of the three subdivisions of the cerebellum exhibit characteristic signs. abduction. decomposition of movements. also will have some amnesia and “cerebellar speech”. Inputs from the cerebrum 1st go through the pontine nucleus (they don’t go straight to the cerebellum).so lesions result in dysmetria.receive sensory inputs from trigeminal and spinalproprioception from the spinocerebellar tract. Tend to fall towards the site of the lesion. In the case of the spinocerebellum.it will usually end at the lateral hemisphere of the cerebellum.

the primary motor area.3a) Functional localisation of motor areas. Broca's aphasia often occurs as a result of strokes. slurred speech). leading to Broca’s aphasiahence he has non-fluent aphasia. in the left frontal lobe. 45. area 44. likely to be the middle cerebral @ that is lesioned. Not so impt to know the blood supply. There is also the premotor area. hands is located closer to the lateral sulcus. lesioning of Wernicke’s area leads to fluent aphasia. The lesion is probably involving the Broca’s area.located in the Broca’s area.located in the Wernicke’s area. Note that it is unlikely to be a Wernicke’s aphasia. The area for the face.thus leading to not just aphasia. but also dysarthria due to psuedobulbar palsy (so thick. 3b) Motor speech area. . lesioning of the arcuate fasciculus connecting the Broca’s and Wernicke’s areas leads to problems with repetition. but more importantly to know the area of defects. mouth. area 22. usually it is the left hemisphere. but is acutely aware of his problem “telegraphic speech”. and also inability to grasp sarcasm.lesions result in aprosodias.there is the somatotopic arrangement along the precentral gyrus. Most lesions that involve Broca's area also involve the neighboring motor cortex. The equivalent of the Broca’s and Wernicke’s areas in the right hemisphere is essential for understanding the emotional nuances and tone. etc. and generalised lesions lead to anomic aphasia. in the left frontal lobe. rhythm of speech (prosody).lesioning leads to receptive aphasia. The lesion also extends to the primary motor cortex. with the arm more affected than the leg. Handedness.relates to which cerebral hemisphere is dominant. Lesioning of Broca’s area results in non-fluent aphasia. probably involving the upper limb area and maybe some part of the face as well. as clearly he can understand verbal commands and ideomotor apraxia is unlikely. Sensory speech area. most commonly affecting the middle cerebral artery territory.lesioning leads to expressive aphasia. 3c) In this example. Patients are often hemiplegic. the area for the legs is located closer to the midline between the hemispheres. and the supplementary motor area.

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