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

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

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

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

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

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

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