Neuroanat- Stroke (Visual, Cerebellum, Speech Areas) | Cerebellum | Parietal Lobe

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. Core ischemic zone Neurons in the core ischemic zone die due to ischemia. 2. there are two major zones of injury: 1.g. Ischemic penumbra . and their excitatory neurotransmitters are released to the environment.

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

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

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

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

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