Neuroanatomy and Neurolocalization of Cerebrum Blen M.( NR-2) Moderator Dr. Amanuel Jan,2021
Content Micro and Macro Anatomy of cerebral hemispheres Cerebral white matter Neuronal networks Vascular neuroanatomy Neurolocalization and Hemispheric specialization
Introduction Clinical diagnosis in neurology requires r ecognition of impaired function, the site of the nervous system affected and what the lesion is. The pattern of structures is relatively constant from person to person which makes localization possible Lesion localization in the cerebral hemispheres relies on the understanding of the function of different portions of the cerebral cortex.
The Cerebral Hemisphere The paired cerebral hemispheres derive from the telencephalon Contains approximately 20 billion neurons spread over an area of 2.5 m2 The cortex is thrown in to folds called gyri and in between are the sulci Its thickness varies from 4.5 mm in the precentral gyrus to 1.3 mm near the occipital pole
Why do women multitask better than men? The corpus callosum is larger in women than in men and contains more neural pathways This is thought to make women superior in processing language, information, emotion and cognition The inferior-parietal lobe is larger in men and it control characteristics that make a person more prone to mechanical and analytical thought
Neocortex (new cortex) - 6 layers a. Ideotypic cortex - 1° motor and sensory cortex b. Homotypic cortex - association areas Mesocortex (middle cortex) - 3-6 layers - related to limbic system a. Cingulate gyrus b. Para hippocampal gyrus Allocortex (other cortex) - 3 layers a. Archicortex - hippocampal formation b. Paleocortex – olfactory area
The Gross Anatomy of the Cerebral Hemispheres The two hemispheres are Separated by a longitudinal cerebral fissure Superolateral surface are separated by two large sulci Sylvian fissure Rolandic or central sulcus Two imaginary lines From upper end of parieto-occipital sulcus to parieto-occipital notch Backward continuation of the lateral sulcus to meet the first imaginary line
Covered by thin grey matter (2-4mm) Three poles Frontal pole anteriorly Occipital pole posteriorly Temporal pole Surfaces Superolateral surface Medial surface Inferior surface
The four lobes are Frontal lobe Parietal lobe Temporal lobe Occipital lobe Other, sometimes designated as a lobe because their parts are interconnected functionally Insula Limbic lobe
Broadmann’s Map These areas were defined and numbered by korbinian broadmann Based on the cortical cytoarchitectonic organisation of neurons Many of the broadmann’s areas are defined on neurological function correlated closely to diverse cortical functions
Frontal lobe The largest of the 4 major paired lobes of the brain, 38% of human brain Lateral view; central sulcus and Sylvain fissure separates it from adjacent lobes Medial view ; Cingulate sulcus-separates the cingulate gyrus from the first frontal and paracentral gyri Inferior view Orbital surface of the prefrontal area
Frontal Lobe
It is divided in to 3 functional areas The primary motor area (area-4) The premotor area (areas 6, 8, 44, & 45) The prefrontal cortex (areas 9-12)
Prefrontal cortex (BA 9-12,32,45-47) Frontal lobe anterior to premotor area Connections : With the Hypothalamus, thalamus, limbic system, motor areas, the temporal and occipital lobes Has three clinically important divisions DLPFC (dorsolateral prefrontal cortex) MPC (medial prefrontal cortex) OFC (orbitofrontal cortex)
Functions DLPFC Organization of tasks ,execution, problem solving, personality, affect and decision making MPC Important in auditory and visual associations OFC Connection with the limbic system, Including the amygdala Frontal eye field control movement of the eyes to the contralateral side Motor speech areas( Broca’s )(BA 44,45)
Lesions Stimulation Psedoseizure like pedaling and thrusting Aversive seizure Frontal eye field Destructive lesions cause gaze deviation ipsilaterally Epileptiform activity cause gaze deviation to the contralateral side Broca’s Aphasia Unilateral- imitation and utilization behavior
Frontal motor areas 1. Primary motor cortex(BA 4) Contains large motor neurons ( Betz cells ) giving tracts to Corticospinal Corticobulbar Motor Homunculus Crossed and inverted representation of the body according to the motor value
Function Initiation of voluntary, fine, discrete (separate) mov´t of limbs. ( eg . Hands, fingers) on opposite side Facilitation of stretch reflex i.e Facilitation of skeletal muscle tone and tendon jerk Lesions Irritative; focal seizure Destructive ; contralateral Flaccid paralysis Loss of deep and cutaneous reflexes in the opposite side
2. Pre motor Receives afferents from other areas of the cortex and projects to the motor cortex and the motor thalamus Involved in the planning and execution of movements, particularly sequences of movements Some fibers descend and make up part of the extrapyramidal system 3. The SMA (Supplementary motor cortex) consists of areas of cortex lying on the medial aspect of the hemisphere Involved coordinating sequence of actions provided from memory
Lesions Stimulation Tonic posturing with or without automatism Destructive Increase in muscle tone & muscle spasticity than weakness Exaggerated tendon jerk Reappearance of primitive reflex Motor aphasia and apraxia Agraphia: failure of writing & drawing skills due to lesion to exner´s center
Q1 . Why do patients with UMNLs tend to have muscle spasticity and increased tone? The EPF transmit inhibitory impulses that lower muscle tone Destruction of the secondary motor area removes the inhibitory influence, and consequently, the muscles become spastic Q2 . What kind of plantar response do we expect with lesions in the primary motor area A positive Babinski´s sign in the opposite side with only dorsiflexion of big toe due to lesion of pyramidal fibers ( no fanning occurs in other fingers b/c extra pyramidal tracts are intact)
Bilateral Frontal lobe lesions Akinetic mutism Gait apraxia Incontinence Perseveration Lack of judgement and foresight Aspontaneity and lability
Parietal lobe The parietal lobe lies posterior to the central sulcus, anterior to the occipital lobe and superior to the temporal lobe. Five principal parts: The postcentral gyrus The posterior portion of the paracentral lobule The superior parietal lobule The inferior parietal lobule The precuneus
1. The primary somatosensory cortex (S1) (BA 3, 1, 2) Lies between the central sulcus and the postcentral sulcus Granular cortex densely packed with stellate cells Sensations derived from skin are appreciated in anterior part of the area and proprioceptive sensations in posterior part of the area If lesions occur without involving thalamus, sensations are perceived but discriminative functions are lost If thalamus also affected, loss of sensations in opposite side of body
2. Secondary sensory area/ SII Situated in post central gyrus Receives sensory impulses from primary sensory area and thalamus Neurons in anterior part respond to touch whereas neurons in posterior part can be excited by touch, auditory, visual and nociceptive stimuli 3. Sensory association areas (BA 5,7,40) • Neurons which react to passive or active rotation of a joint or joints • Higher association area, concerned with stereognosis
4. The Precuneus Is an area of the cortex just anterior to the occipital lobe on the medial hemispheric surface Involved in visuospatial imagery, episodic memory retrieval
Lesions Unilateral lesion( Either Hemisphere) Loss of Cortical Sensations Loss fine touch more than pain Hypotonia, muscle atrophy, and pseudoataxia Lower quadrantanopia Bilateral lesion: Severe Constructional Apraxia Optic Ataxia
Case-1 A 78 years old female presents with an acute onset of confusion, lately she had a difficulty of doing her bill's with simple mathematical calculation, she had a difficulty of reading a written language . She went to doctor and On examination there is impaired right left orientation, arithmetic abilities and finger identification MRI shows severe foci of cortical and subcortical increased T2 signals the most probable diagnosis is??
Gerstmann’s syndrome Combination of the tetrads of Acalculia, Dysgraphia, Finger anomia and Right-left disorientation Left Inferior parietal lobe damage
Temporal lobe Situated inferior to the lateral fissure and anterior to the parieto-occipital sulcus Contains three gyri, separated by two sulcus Superior gyrus - auditory and language functions Middle and inferior gyri -integration of vision Hippocampal formation Learning and memory Amygdala; emotions(fear, anger…)
1. Primary auditory cortex (areas 41 and 42) The transverse temporal gyri (of Heschl) Buried in the Sylvain fissure at the posterior end of the superior temporal gyrus on its dorsal surface Hearing is bilaterally represented but there is contralateral dominance 2. The auditory association cortex(Area 22) Found immediately adjacent to the primary auditory cortex Differentiate and interpret sounds 3. Wernicke’s speech Area (Area 22) Posterior superior temporal area , in the dominant hemisphere
Occipital lobe A small part of the dorsolateral surface of the hemisphere It rests on the tentorium cerebelli It is separated on medial surface from parietal lobes by parieto-occipital fissure The lateral occipital sulcus, divides the lobe into superior and inferior occipital gyrus The calcarine fissure separates the medial surface into the cuneus above and the lingual gyrus below
Primary visual cortex(BA 17) At the lip of the calcarine Receives primary visual impressions as Color, size, form, motion and illumination Receives fibers from the temporal half of the ipsilateral retina and the nasal half of the contralateral retina Lesions Stimulation- visual hallucination, scotoma and flash of lights Destructives- visual field defect, usually macular sparing hemianopia Bilateral lesions- Cortical blindness Bilateral hemianopia, scotoma Anton's hallucination syndrome
2. Visual Association Area – (Area18 & 19) Recognition and identification of objects and store visual memories Area 18- receive stimulus from the primary visual cortex Area 19- connects with the entire cortex Lesions- Contralateral disconnection syndrome, visual inattention Unable to localize himself or objects in space 3. Fusiform and lingual gyri Color vision and face recognition Lesions- Prosopagnosia
The Limbic lobe Sometimes considered a separate lobe of the brain, because of its function than its anatomy A ring of cortex on the medial aspect of each cerebral hemisphere and includes The cingulate gyrus The Para hippocampal gyrus The hippocampus: The mammillary bodies (part of the hypothalamus); The anterior nucleus of the thalamus;
Functions This system participates in the control of autonomic function, arousal, motivated behavior, emotion, learning, and homeostasis Lesions A disturbance in this function is known as an amnestic state. And it can be Anterograde, retrograde or global.
Primary Cortical Fields
Cerebral White Matter A central core of white matter that forms the bulk of the cerebrum and represents fiber tracts Supported by Neuroglia, carrying information destined for the cortex and Cortical responses to other regions of the CNS There are three types of fibers based on their orientation
Association fibers Connect one area of cerebral cortex with another area in the same hemisphere Commissural fibers , Connect areas of the cerebral cortex in opposite hemispheres Main ones are Corpus callosum, anterior commissure and the hippocampal commissure Projection fibers Project to deep structures, like the thalamus
Q. What is their clinical importance? Characteristics of white matter lesions are Weakness Spasticity Visual field deficits “Pure” motor syndromes Urinary incontinence Lesions cause symptoms that are referable to the cortical region giving rise to the white matter tract involved
Neural networks Five anatomically defined large-scale networks are most relevant to clinical practice: 1. P erisylvian network for language, 2. P arietofrontal network for spatial orientation, 3. O ccipitotemporal network for face and object recognition, 4. L imbic network for retentive memory, and 5. P refrontal network for the executive control of cognition and comportment.
1. The perisylvian network for language
Aphasia Aphasia is a defect in language processing caused by damage to any one of the neural network component In ~ 90-95% of right-handers and 60-70% of left-handers, aphasia occurs only after lesions of the left hemisphere.
Wernicke’s Aphasia Markedly impaired comprehension, Impaired naming and repetition Normal fluency, prosody, and grammatical structure. Writing and Reading: similarly affected Prognosis for recovery of language function is guarded 2. Broca’s Aphasia Intact comprehension Decreased fluency, Impaired repetition Marked naming difficulties
3. Conduction Aphasias Normal fluency and normal comprehension, but impaired repetition Interruption at the arcuate fasciculus or other pathways in the vicinity of the supramarginal gyrus that connect Wernicke’s area to Broca’s area 4. Transcortical Aphasias Resemble Broca’s, Wernicke’s, and global aphasias, except that repetition is spared Classic cause: watershed infarcts Three types; Motor (non fluent) type, Sensory (fluent) aphasia and mixed
6. Global Aphasia The combined dysfunction of Broca’s and Wernicke’s areas All modalities of speech are impaired from strokes that involve the entire MCA distribution in the left hemisphere 6. Subcortical Aphasia Subcortical components of the language network including Thalamus and Basal ganglia Combinations of deficits but rarely fit the specific patterns
Do we expect Aphasia in right hemispheric lesion??? First , right-handed patients occasionally become aphasic after right hemisphere strokes, a phenomenon called crossed aphasia . Second left-handed patients may have right hemisphere language dominance Third, even right-handed persons with typical left hemisphere dominance for language have subtly altered language function after right hemisphere damage
Role of the nondominant hemisphere in language? Important in both the recognition and the production of the affective elements of speech. Lesions: difficulty judging the intended expression imparted by a particular tone of voice, or they may have difficulty producing emotionally appropriate expression in their own voice. In lesions of the dominant hemisphere, callosal connections may allow the nondominant hemisphere to take over some functions of the damaged areas and to participate in at least partial recovery
2. The prefrontal network for Attention & Behavior Prefrontal network: Prefrontal Cortex (motor-premotor, dorsolateral , medial , and orbitofrontal components) Subcortical Structures (the head of the caudate and the dorsomedial nucleus of the thalamus). Important role: integration of thought with emotion & motivation .
Lesions Frontal Abulic Syndrome (DLPFC); loss of initiative, curiosity, creativity, emotional blandness, apathy and lack of empathy. Frontal Disinhibition Syndrome (medial/orbitofrontal): severe impairments of judgment, insight, foresight, and the ability to mind rules of conduct. Fontal release signs (grasping, sucking ) These syndromes tend to arise almost exclusively after bilateral lesions .
Phineas Gage (1823–1860) Railroad construction man, Sustained metal injury with accidental frontal lobectomy. He became unreliable, with temperament changes hypesexuality, poor social interaction but with preserved intellectual function
3. The Parietofrontal Network For Spatial Orientation Network for directed attention to extra personal space includes: Cortical components The posterior parietal lobe Frontal eye fields Cingulate gyrus and their connections Subcortical components : striatum and thalamus Lesions Hemispatial neglect, Simultanagnosia and object finding failures.
Q. Why does right hemispheric lesions cause Hemineglect?? The right hemisphere directs attention within the entire extra personal space, whereas the left hemisphere directs attention mostly within the contralateral right hemi space
Case -2 A 68 years old male who had a difficulty of finding where the door is and where the wall ends, after he wakes up from sleep. He first thought he did not have a good night sleep he stretch out to find his telephone but couldn’t find it out, one of his family members point it out and it was right next to him where he left it the eye doctor told him that his vision is quite normal despite the fact he hardly find the way out form the doctors office what is happening to the patient ??
Balint’s Syndrome Bilateral involvement of the network for spatial attention, especially its parietal components Components of Balint’s syndrome are:- O culomotor apraxia O ptic ataxia , and S imultanagnosia Etiology: CVA, hypoglycemia, sagital sinus thrombosis, Alzheimer’s disease
Case 3 A 65 year old male patient come to you with complaint of sudden failure to recognize his Son by looking at his face whom he recognized later as he conversed to him. His Ophthalmologist confirmed that he doesn’t have eye problems. He still complains that he recognizes his son only hearing his voice and looking his clothing .
4. Occipitotemporal network Prosopagnosia patients are unable to recognize people by looking at their faces The usual lesion location is the bilateral inferior occipitotemporal cortex , also known as the fusiform gyrus Achromatopsia A central disorder of color perception. Others- Micropsia, Macropsia, Metamorphopsia, Visual reorientation :
5. The Limbic Network for Memory Includes Limbic and paralimbic areas The anterior and medial nuclei of the thalamus, The medial and basal parts of the striatum, and The hypothalamus Function Memory Immediate (working, Short-term (recent) and Long-term (remote) memory Disturbance Amenesia Could be ;Retrograde amnesia, Anterograde amnesia or Confabulation
VASCULAR NEUROANATOMY
The arterial supply is derived from the anterior circulation provided by the bilaterally paired internal carotid arteries, as well as by the posterior circulation provided by the bilateral vertebral arteries These anterior and posterior circulations meet in an anastomotic ring called the circle of Willis, from which all major cerebral vessels arise The main arteries supplying the cerebral hemispheres are the anterior, middle, and posterior cerebral arteries.
ACA Supply – frontal to anterior parietal lobe area Lesions Contralateral weakness leg more than the arm or face with cortical sensory loss transcortical motor aphasia contralateral neglect grasp reflex, impaired judgment, flat affect, apraxia, abulia, and incontinence “alien hand syndrome”
MCA Supply the dorsolateral cortex Lesions are more common than ACA or PCA areas Contralateral weakness arm and face more than leg with cortical sensory loss and gaze preference toward the side of the lesion global aphasia, contralateral homonymous hemianopia hemineglect, apraxia and anosognosia
PCA Supply inferior and medial temporal occipital lobe Infraction typically cause a contralateral homonymous hemianopia Also cause visual field defects , color anomia and paresthesia without any motor findings Alexia without agraphia
Superficial and Deep Blood Supply to the Cerebral Hemispheres
Watershed zones Regions between cerebral arteries in both the ACA–MCA and MCA–PCA zones A sudden occlusion of an internal carotid artery or a drop in blood pressure in a patient with carotid stenosis can cause an ACA–MCA watershed infarct Infarcts can produce proximal arm and leg weakness (“man in the barrel” syndrome), transcortical aphasia syndromes MCA–PCA watershed infarcts can cause disturbances of higher-order visual processing
VASCULAR NEUROANATOMY VEINS The superficial veins drain mainly into the superior sagittal sinus and the cavernous sinus, while the deep veins drain into the great vein of Galen then reaches the internal jugular veins. Sagittal sinus thrombus and other venous thrombus are the common conditions
Principles of Cerebral Localization and Lateralization Q. How are cortical lesions different from sub-hemispheric lesions? Neuroplasticity and redundant pathway Extensive neural networks The result is: Less pronounced deficits with lesions caused a major motor or sensory disturbance if occurs in the subcortical structures Single lesions may be clinically silent and become symptomatic when additional lesions impair the function of the network
Cortical vs. subcortical lesions can sometimes be differentiated clinically based on the absence or presence of so called cortical signs These include Aphasia Neglect Seizures Homonymous visual field defects and Cortical sensory loss However, each of these deficits can be seen in some cases of subcortical lesions as well
Case -4 A 23-year-old woman with a 4-year history of epileptic attacks visited her neurologist. Her families described one of her attacks. For a few seconds before the convulsions began, the patient would complain of an unpleasant odor, similar to that encountered in a cow shed. This was followed by a shrill cry as she fell to the floor unconscious. Her whole body immediately became involved in generalized tonic and clonic movements.
Anatomic location General characteristics of seizures Frontal lobe Usually occur several times per day, short in duration, during sleep. Complex gestural automatisms is common at onset. Tonic/postural manifestation is prominent. Occipital lobe Usually simple partial and secondarily generalized seizures. include visual symptoms that are contralateral to cortex: Positive visual manifestations include sparks, flashes, and Negative visual manifestations include scotoma, hemianopsia, and amaurosis. Parietal lobe Most are simple partial but can secondarily generalize. In the dominant parietal lobe , language is often involved. Sensory features: Positive symptoms include tingling and electric feeling. Negative symptoms include numbness, absent body part, and asomatognosia. Temporal lobe Simple partial seizures: autonomic/ psychic symptoms and sensory phenomena: olfactory, auditory, and (most commonly) rising epigastric sensation. Complex partial seizures: alteration in consciousness with behavioral arrest, often followed by oroalimentary or hand automatisms. Postictal confusion is usually followed by amnesia of the event. Clues to anatomic location of a seizure
Hemispheric Specialization Many basic sensory and motor functions in the brain are distributed symmetrically For unknown reasons, however, there are marked asymmetries in several brain functions Cerebral dominance is related to handedness and anatomic differences between the hemispheres
Handedness The most obvious asymmetry in cerebral function is handedness . Approximately 90% of the population is right-handed Lesions of the dominant hemisphere therefore are more commonly associated with apraxia , a disorder of formulating skilled movements Language Another well-known example of hemispheric specialization. The left hemisphere is dominant for language in over 95% of right-handers, and in over 60 to 70% of left-handers
Anteroposterior Organization In addition to left versus right, brain functions are also organized along the anterior to posterior axis More posterior regions are sensory and more anterior regions are motor The posterior parietal and temporal association cortex are more involved in interpreting perceptual data and assigning meaning to sensory information The anterior frontal association cortex is more important for planning, control, and execution of actions
References Dejong’s the neurologic examination, 8 th edition W. Brazis, Localization in clinical neurology, 6 th edition Snells clinical neuroanatomy,7 th edition Grays the anatomic basis of clinical practice, 39 th edition Blumenfeld Neuroanatomy through clinical cases, 2 nd edition