Cerebral hemisphere | Anatomy2Medicine
general-appearance-of-the-cerebral-hemispheres

Cerebral hemisphere

    • The Cerebral Cortex
      • contains 20 billion nerve cells.
      • consists of the neocortex (90%) and the allocortex (10%).

 

  • Neocortex (isocortex; homogenetic cortex)

 

        • is a six-layered cortex.

 

  • Allocortex (heterogenetic cortex)

 

        • is three-layered and includes two types

 

  • Archicortex

 

          • includes the hippocampus and the dentate gyrus.

 

  • Paleocortex

 

          • includes the olfactory cortex.
    • Six Layers of the Neocortex
    • are expressed as roman numerals I through VI:
      • Molecular layer (I)
      • External granular layer (II)
      • External pyramidal layer (III)
        • gives rise to association and commissural fibers.
      • Internal granular layer (IV)
        • receives thalamocortical fibers from the thalamic nuclei of the ventral tier (e.g., VPL,  VPM nuclei).

 

  • in the striate cortex (area 17), receives input from the lateral geniculate body.
  • myelinated fibers of this layer form the stripe of Gennari, which is visible to the naked eye.

 

      • Internal pyramidal layer (V)
        • gives rise to corticobulbar, corticospinal, and corticostriatal fibers.
        • contains the giant cells of Betz

 

  • giant cells of Betz are found only in the motor cortex (area 4) of the precentral gyrus and the anterior paracentral lobule.

 

      • Multiform layer (VI)
        • is the major source of corticothalamic fibers

 

  • Functional Areas of the Cerebral Cortex

 

      • is divided into 47 cytoarchitectural areas, the Brodmann areas.
      • Sensory areas

 

  • Primary somatosensory cortex (areas 3, 1, and 2)

 

          • is located in the postcentral gyrus and in the posterior part of the paracentral lobule
          • receives input from the ventral posterior nucleus.
          • contributes to the corticospinal tract.
          • is somatotopically organized as the sensory homunculus
          • Stimulation results in contralateral numbness and tingling (paresthesia).

 

  • Destruction results in a contralateral loss of tactile discrimination (hypesthesia and astereognosis).
  • Secondary somatosensory cortex
  • Present along the superior bank of the lateral sulcus.
  • Somatosensory association cortex
  • Superior parietal lobule (areas 5 and 7)

 

          • receives input from areas 3, 1, and 2.
          • Area 7 receives visual input from area 19.
          • Destruction results in
            • contralateral losses of tactile discrimination
            • stereognosis (the ability to recognize form)
            • statognosis (the ability to recognize the position of body parts in space)
            • neglect of events occurring in the contralateral portion of the external world

 

  • more commonly seen with parietal damage on the right side
  • Supramarginal gyrus (area 40)

 

          • interrelates somatosensory, auditory, and visual input (multimodal sensory stimuli).
          • Destruction in the dominant hemisphere may result in the following deficits:

 

  • Ideomotor or “classic” apraxia (ideokinetic apraxia)
  • is the inability to button one’s clothes or comb one’s hair when asked.

 

              • Is the inability to manipulate tools,with retention of the ability to explain their use.

 

  • Ideational or sensory apraxia

 

              • is characterized by the inability to formulate the ideational plan for executing the several components of a complex multistep act (e.g., performing the steps of lighting a cigarette when asked to do so).
              • occurs most frequently in diffuse cerebral degenerating disease

 

  • Alzheimer disease,

 

                • multi-infarct dementia.

 

  • Facial apraxia

 

              • Is the inability to perform facial–oral movements on command (i.e.,lick the lips).
              • is the most common apraxia.

 

  • Conduction aphasia

 

              • is associated with poor repetition of spoken language

 

  • results from interruption of the arcuate
  • Primary visual cortex (area 17)

 

          • is located in the occipital lobe in both banks of the calcarine sulcus.
          • receives input from the lateral geniculate body.

 

  • Destruction results in contralateral homonymous hemianopia
  • Secondary and tertiary visual cortices

 

          • include areas 18 and 19 of the occipital lobe
          • Lesions may result in visual hallucinations.
        • Visual association cortex (angular gyrus [area 39])
          • receives input from areas 18 and 19.

 

  • Destruction of the underlying visual radiation results in contralateral homonymous hemianopia or lower quadrantanopia.

 

          • Destruction in the dominant hemisphere results in Gerstmann syndrome with the following deficits:

 

  • Right–left confusion

 

            • Finger agnosia
              • inability to recognize, name, or select one’s own or another’s fingers
            • Agraphia
              • inability to express thoughts in writing

 

  • with possible retention of the ability to copy written or printed words

 

              • often coexists with alexia
            • Dyscalculia
              • difficulty with arithmetic

 

  • Primary auditory cortex (areas 41 and 42)

 

          • is located in the transverse gyri of Heschl.
          • receives input from the medial geniculate body.

 

  • unilateral destruction results in only partial deafness (due to bilateral cochlear representation).
  • Auditory association cortex (area 22)

 

          • is located in the posterior part of the superior temporal gyrus.
          • includes Wernicke speech area.

 

  • includes the planum temporale (part of Wernicke speech area), which is larger in the dominant hemisphere.

 

          • Lesion in the dominant hemisphere results in Wernicke sensory aphasia.

 

  • Lesion in the nondominant hemisphere results in sensory dysprosody

 

            • inability to perceive the pitch or rhythm of speech

 

  • Gustatory cortex (area 43)
  • is located in the parietal operculum and parainsular cortex.
  • receives taste input from the VPM nucleus of the thalamus.
  • Vestibular cortex (area 2)

 

      • is located in the postcentral gyrus.
      • receives input from the ventral postero inferior (VPI) and the VPL nuclei of the thalamus.
    • Motor areas

 

  • Primary motor cortex (area 4)

 

        • is located in the

 

  • precentral gyrus
  • anterior part of the paracentral lobule.

 

        • contributes to the corticospinal tract.
        • is somatotopically organized as the motor homunculus
        • contains the giant cells of Betz in layer V
        • Stimulation results in contralateral movements of voluntary muscles, especially distal muscles of the limbs.

 

  • Ablation results in a contralateral upper motor neuron (UMN) lesion.

 

        • Bilateral lesions of the paracentral lobule (e.g., parasagittal meningiomas) result in urinary incontinence.

 

  • Premotor cortex (area 6)

 

        • is located anterior to the precentral gyrus.
        • contributes to the corticospinal tract.
        • plays a role in the control of proximal and axial muscles
        • it prepares the motor cortex for specific movements in advance of their execution.
        • Stimulation results in

 

  • adversive movements of the head and trunk

 

          • flexion and extension of the extremities.
        • Lesions in the dominant hemisphere cause
          • sympathetic apraxia
          • motor apraxia in the left hand

 

  • Supplementary motor cortex (area 6)

 

        • is located on the medial surface of the hemisphere anterior to the paracentral lobule.
        • contributes to the corticospinal tract.
        • plays a role in
          • programming complex motor sequences
          • coordinating bilateral movements
          • it regulates the somatosensory input into the motor cortex.
        • Stimulation results in
          • vocalization with associated facial movements
          • coordinated movements of the limbs.
        • Ablation in human subjects has resulted in transient speech deficits or aphasias.
        • Bilateral lesions result in hypertonus of the flexor muscles but no paralysis

 

  • Frontal eye field (area 8)
  • is located in the posterior part of the middle frontal gyrus.
  • projects via the corticotectobulbar tract to the contralateral lateral gaze center of the pons (abducent nucleus).

 

        • Stimulation (irritative lesion) results in conjugate deviation of the eyes to the opposite side.

 

  • Destructive lesions resulting conjugate deviation of the eyes toward the side of the lesion.

 

    • Areas of higher cortical function

 

  • Prefrontal cortex (areas 9–12)

 

        • extends from area 6 to the frontal pole (area 10).
        • has reciprocal connections with the mediodorsal nucleus of the thalamus.

 

  • Frontal lobe syndrome (Phineas Gage syndrome)

 

        • results from lesions of the prefrontal cortex.
        • results in the following signs
          • Inappropriate social behavior
            • Lesions usually involve the fronto-orbital prefrontal cortex.

 

  • Difficulty in adaptation and loss of initiative

 

            • Lesions involve the dorsolateral prefrontal cortex

 

  • Sucking, groping, and grasping reflexes

 

          • Gait apraxia

 

  • Incontinence

 

          • abulia (loss of the ability to perform voluntary actions)
          • akinetic mutism (a coma-like state called coma vigil)

 

  • These signs result from bilateral disease.
  • Broca speech area (areas 44 and 45)
  • is located in the posterior part of the inferior frontal gyrus in the dominant hemisphere.

 

        • is connected to Wernicke speech area by the arcuate fasciculus.

 

  • Broca aphasia

 

          • results from lesions in Broca speech area.
          • is also called motor, expressive, nonfluent, or anterior aphasia.
          • causes patients to speak slowly (nonfluent) and with effort
          • they have good comprehension of spoken and written language.
          • is frequently accompanied by
            • contralateral weakness of the lower face and arm

 

  • sympathetic apraxia of the left hand (the inability to write with the nonparalyzed hand).
  • Wernicke speech area (area 22)
  • is located in the posterior part of the superior temporal gyrus in the dominant hemisphere.

 

        • is connected to Broca speech area by the arcuate fasciculus.

 

  • Wernicke aphasia

 

          • results from lesions in the dominant hemisphere.
          • is also called sensory, receptive, fluent, or posterior aphasia.
          • Patients have poor comprehension of speech, speak faster than normal
          • Patients have difficulty in finding the right words to express themselves
          • They appear unaware of the deficit.

 

  • Arcuate fasciculus

 

        • underlies the supramarginal gyrus (area 40) and the frontoparietal operculum.

 

  • connects the audiovisual association areas (areas 22, 39, and 40) with Broca speech area (areas 44 and 45).
  • Conduction aphasia

 

          • results from transection of the arcuate fasciculus.
          • is a fluent aphasia associated with poor repetition of spoken language
          • Speech comprehension and expression are relatively good.
          • Paraphrasic errors (using incorrect words) are common
          • object naming is impaired (nominal aphasia or amnestic aphasia)
          • Patients are aware of the deficit.
      • Corpus callosum
        • interconnects corresponding hemispheric areas.
        • does not contain commissural fibers from the
          • hand region of the motor or sensory strips

 

  • striate cortex.

 

        • receives its blood supply from the anterior cerebral artery and the posterior cerebral artery
        • splenium is perfused by the posterior cerebral artery

 

  • Damage to the splenium results in left hemidyslexia

 

    • Cerebral dominance
      • Dominant hemisphere
        • is responsible for propositional language consisting of grammar, syntax, and semantics
        • is also responsible for speech and calculation.
        • The left hemisphere is dominant in 95% of cases.
        • Lesions of the dominant superior parietal lobule
          • result in contralateral loss of sensory discrimination (astereognosis) (i.e., loss of dorsal column modalities; area 5).
          • result in contralateral neglect (area 7).
        • Lesions of the dominant inferior parietal lobule
          • involve the supramarginal and angular gyri (areas 40 and 39).
          • result in the following conditions:

 

  • Receptive aphasia
  • Gerstmann syndrome

 

            • Alexia with agraphia (often coexists with Gerstmann syndrome)
            • Tactile agnosia (bimanual astereognosis)

 

  • Ideomotor apraxia
  • Ideational apraxia

 

      • Nondominant hemisphere
        • is primarily responsible for
          • three-dimensional or spatial perception

 

  • nonverbal ideation (music and poetry).

 

        • Lesions of the nondominant superior parietal lobule
          • result in contralateral loss of sensory discrimination (i.e., loss of dorsal column modalities; area 5).
          • result in contralateral neglect (area 7).
        • Lesions of the nondominant inferior parietal lobule
          • involve the supramarginal and angular gyri.
          • result in the following conditions:

 

  • Left-sided hemineglect

 

            • results in a lack of awareness of the left half of space or the left half of the body.
          • results in hemi-inattention or extinction

 

  • if, with the patient’s eyes closed, both hands are touched simultaneously, the left hand stimulus often is not reported.
  • Topographic memory loss

 

            • results in the inability to negotiate familiar surroundings.

 

  • Anosognosia (denial of deficit)

 

            • results in indifference to the causal disease (e.g., hemiparesis or hemianopia).
          • Constructional apraxia

 

  • results in the inability to draw simple designs (e.g., cross, star, or clock)

 

            • the left side of the design is omitted.

 

  • may also occur in lesions of the dominant hemisphere.
  • Dressing apraxia

 

            • results in the inability to dress oneself.

 

  • Lesions of the nondominant inferior frontal gyrus (areas 44 and 45)

 

          • correspond to Broca speech area
          • result in expressive dysprosody (the inability to articulate the pitch and rhythm of speech).

 

  • Lesions of the nondominant superior temporal gyrus (area 22)

 

          • correspond to Wernicke speech area

 

  • result in receptive dysprosody (the inability to perceive pitch and rhythm of speech)