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

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

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

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

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

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