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

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

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

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

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

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

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