Traverse : These relay impulses from the spinothalamic tracts medial lemnisci and….

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The meninges lie immediately deep to the inner surface of the skull and constitute the membranous covering of the brain.

The pericranium of the inner surface of the skull and the dura mater are collectively termed the pachymeninges, while the pia mater and arachnoid membrane are the leptomeninges.

Between the dura mater and the arachnoid is the (normally only virtual) subdural space; between the arachnoid and the pia mater is the subarachnoid space.

The subarachnoid space contains the cerebrospinal fluid (CSF).

The functions of CSF are physical (compensation for volume changes, buffering and equal distribution of intracranial pressure despite variation in venous andarterial blood pressure) and metabolic (transport of nutrients and hormones into the brain).

The cerebrospinal fluid is formed in the choroid plexuses of the four cere- bral ventricles (right and left lateral ventricles, third ventricle, and fourth ventricle).

It flows through the ventricular system, then enters the subarachnoid space surrounding the brain and spinal cord (external CSF space).

It is resorbed in the arachnoid granulations of the superior sagittal sinus and in the perineural sheaths of the spinal cord. Meningeal syndrome include in neck stiffness (passive flexion of the neck is restricted and painful), Kernig sign (resistance to passive extension of the knee while the hip is flexed), attempts at neck flexion, pressing the pubis may induce flexion of the hip or knee Brudzinski signs (upper, middle).

Passive extension of the knee may induce flexion of the opposite hip or knee.

And general cerebral signs (headache, vomiting, nausea, general hyperesthesia, seizures and changes of consciousness). What is meningism? It’s a condition in which the symptoms simulate meningitis, but in which no actual inflammation of these membranes is present. The functional organization of the cerebral cortex can be studied with various techniques: direct electrical stimulation of the cortex during neurosurgical procedures, measurement of cortical electrical cortical activity (electroencephalography and evoked potentials), and measurement of regional cerebral blood flow and metabolic activity.

Highly specialized areas for particular functions are found in many different parts of the brain.

A lesion in one such area may produce a severe functional deficit, though partial or total recovery often occurs because adjacent uninjured areas may take over some of the function of the lost brain tissue. (The extent to which actual brain regeneration may aid functional recovery is currently unclear.) The specific anatomic patterns of functional localization in the brain are the key to understanding much of clinical neurology. Lesions of the Frontal Lobe The motor and premotor function.

Primary motor cortex (somatic motor area) are located in precentral gyrus.

This region includes the giant pyramidal cells of Betz in layer V; at this site the gray matter is of maximum thickness.

The motor area gives rise to impulses that initiate volitional movements on the opposite side of the body.

It is subdivided into centers; each of these preferentially controls muscles that govern movements of individual parts of the opposite half of the body.

It is somatotopically organized.

These are represented in inverted order.

Destruction of this area caused paresis or paralysis of the opposite side of the body.

This paralysis affects predominantly the distal portions of the extremities, and fine, skilled volitional movements are entirely abolished.

Because the larynx, pharynx, palate, trunk muscles, diaphragm, rectum, and bladder are bilaterally innervated, the functions of these structures are little affected with unilateral lesions.

The premotor locates anteriorly of the precentral gyrus and effects opposite half of the body motor control.

It is involved in the planning of movements.

Irritation of the motor (and/or pre-motor) cortex causes focal or jacksonian convulsions. The frontal motor eye field.

Lies anterior to the premotor cortex and controls voluntary movement of the eyes, especially when moving eyes to follow a moving target.

Stimulation of this region results in strong, rapid conjugate deviation of the eyes to the opposite side, which may be accompanied by conjugate movement of the head and rotation of the trunk.

Destruction of this area is followed by paresis of conjugate gaze to the opposite side. The motor speech areas.

The lower portion of the motor and premotor region is known as Broca’s area, or the motor speech area.

Destructive lesions of this region produce an oral expressive type of aphasia. Destruction of the anterior two-thirds of the frontal lobe convexity results in deficits in the following functions: concentration, orientation, abstracting ability, loss of initiative, inappropriative behavior, release of grasping reflexes, gait apraxia and sphicteric incontinenced. Lesions of Parietal Lobe The postcentral region occupies the postcentral gyrus and stretches from the superomedial border to the adjoining part of the paracentral lobule.

There is the typical sensory cortex with all well developed six layers.

The postcentral region is the sensory receptive area.

It receives information from the nuclei ventralis posterolateralis and posteromedialis of the lateral nuclear mass of the thalamus.

These relay impulses from the spinothalamic tracts, medial lemnisci, and secondary trigeminal tracts, and traverse the posterior limb of the internal capsule.

The functions of the parietal lobe are analysis, synthesis, integration, interpretation, and elaboration of the primary sensory impulses that are received from the thalamus.

The sensory cortex is somatotopically organized too.

Destruction of this area results in contralateral hemihypestesia and astereognosis.

Stimulation of this area by either artificial excitation or disease processes produces paresthesias on the opposite side of the body (sensory jacksonian epilepsy). The superior parietal lobule.

Destruction of this lobule results in contralateral astereognosis and sensory neglect. The angular and supramarginal gyri of the dominant hemisphere are important in relation to language and related functions, and lesions in these areas may be responsible for various types of receptive aphasia, alexia, acalculia, and sensory apraxia.

Destruction of nondominant hemisphere result in autotopagnosia or somatotopagnosia (the loss of power to orient the body or the relation of its individual parts; there may be loss of identification of one limb or one part of the body), anosognosia (the ignorance of the existence of disease), pseudomelia (a sensation of presence or absence of additional extremities). Lesions of the Temporal Lobes The auditory receptive region is located in the transverse temporal gyri (Heschl’s convolutions), which lie on the dorsal surface of the posterior part of the superior temporal convolution.

The auditory radiations pass from the medial geniculate body to the auditory receptive region.

Hearing is bilaterally represented in the temporal lobes, although a greater number of impulses may be received from the contralateral ear. Stimulation of the superior temporal gyrus produces vague auditory hallucinations in the form of tinnitus and sensations of roaring and buzzing, and stimulation of adjacent areas causes vertigo and a sensation of unsteadiness.

Unilateral destruction of the transverse temporal gyri does not cause deafness (because of bilateral representation of hearing).

Destruction of Wernicke’s speech area in the dominant hemisphere (posterior part of the superior temporal gyrus) results in a receptive aphasia (Wernicke’s aphasia), in which patient cannot understand any form of language.

Speech is spontaneous, fluent, and rapid but makes little sense. The optic radiations pass through the temporal lobe and curve around the descending horn of the lateral ventricle; lesion of them may cause either a superior quadrantic or hemianopic defect in the visual fields.

Destruction of olfactory tract results in ipsilateral anosmia.

The stimulation of the temporal lobe cortex in epileptic patients gives rise to illusions of perception, olfactory, visual and gustatory hallucinations, dreamy states and reminiscences and automatisms.

Petit mal is a typical symptom of temporal lobe lesion.

These phenomena have been found to be associated with abnormal discharges or pathologic lesions of the anterior and medial portions of the temporal lobes, including the hippocampal gyrus, uncus, amygdaloid complex, and hippocampus, or the subcortical connections of these structures, many of which actually belong to the limbic system.

Hippocampal cortex (archicortex).

Bilateral lesion result in the inability to consolidate short-term memory into long-term memory; earlier memories are retrievable.

Olfactory and gustatory hallucinations are results of the uncus irritative lesion. Lesions of the Occipital Lobe The occipital lobe is more nearly a structural and functional entity than are any of the other cerebral lobes.

All of its functions are concerned either directly or indirectly with vision.

The visual receptive area is located on the lips of the calcarine fissure and adjacent portions of the cuneus and lingual gyrus, and extends around the occipital pole to occupy a portion of the lateral surface of the hemisphere.

The optic radiations pass from the lateral geniculate body to the striate cortex on the upper and lower lips of the calcarine fissure.

Stimulation, or irritation, of the calcarine cortex produces unformed visual hallucinations, such as fotomas and flashes of light, in the corresponding fields of vision.

Destructive lesions result in defects in the visual fields supplied by the affected areas.

Bilateral lesion may result in cortical blindness.

Unilateral lesions may result in contralateral hemianopia or quadrantanopia. Lesions of the Limbic Lobe The hippocampal gyrus, uncus, isthmus, and gyrus cinguli are usually grouped together as the limbic lobe or limbic system.

Closely related are the subcallosal and retrosplenial gyri, pyriform area, hippocampus, and various subcortical structures including the amygdala and septal nuclei.

Certain of these are often included in the temporal lobe, but anatomically and physiologically they are placed in the limbic system, or “visceral brain.” Irritation, or stimulation, of these produces either olfactory or gustatory hallucinations.

These are often very disagreeable and are described with difficulty.

For example, the patient may describe the taste of blood, the odor of burning rubber, or of decaying material.

The hallucinations may be accompanied by smacking or licking of the lips, tasting movements of the tongue, swallowing, and salivation, and constitute an important part of the complex partial seizure.

Destruction of these areas is not followed by loss of smell or taste because of their bilateral connections. The limbic lobe and related structures have rich connections with the hypothalamus and thalamus, and play an important part in the central regulation of the autonomic nervous system.

Abnormal affective and emotional responses, fear and aggressive behavior may be lessened by interruption of the connections between these cortical areas and the thalamus and hypothalamus.

Bilateral or even unilateral lesions or resection of the hippocampus and hippocampal gyrus are followed by marked impairment of recent memory.

Bilateral lesions of the cingulate gyrus cause apathy, akinesia, and mutism. Higher Cortical Functions Disorders This section concerns the more important higher cortical functions and the typical clinical findings associated with their impairment.

An adequate understanding of these very complex functions requires knowledge of certain basic concepts of neuropsychology and neuropsychological testing, which will be briefly explained where necessary.

We will discuss language, aspects of perception, the planning of complex patterns of movement and motor activities, and the control of social behavior.

These functions are mostly subserved by the multimodal association cortices, which make up more than half of the brain surface and which receive afferent input from the primary somatosensory, special sensory, and motor cortices, the mediodorsal and lateroposterior pulvinar portions of the thalamus, and other association areas in both hemispheres.

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