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

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

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

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

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