1. FUNCTIONAL ANATOMY OF THE BRAIN - By Dr. O. C. Ogun Federal Neuropsychiatric Hospital Yaba

2. The brain occupies the cranial vault in animals. It consists of: The cerebrum - which consists of two large cerebral hemispheres, the cerebellum, the midbrain, the pons and The medulla oblongata. Midbrain, pons and medula = the brain stem. Continuous below with the spinal cord. Peripheral nerves attached to the brain are called cranial nerves.

3. Inter hemispheric separation by longitudinal/sagittal fisse Intrahemispheric – central sulcus/fissure of Rolando - Lateral sulcus/sylvian fissure Division of the lobes Convolutions on the surface ^surface area Fissures are deep, sulci define small areas or gyri Grey matter surround central core of white matter (nerve fibres)

4. Fibres 1)Association 2)Projection, e.g. to brainstem 3)Commissural connect identical areas of the two hemispheres e.g. corpus callosum. Cerebral dominance/Hemispheric Lateralization Rule:- Contra lateral hemisphere to dominant hand. Dominant hemisphere mediates language and speech functions

5. But 10% R-handed, R hemispheric dominance Left handedness - 20% R. hemisphere-dominant - 64% L. “ “ - 16% bilateral dominance

6. EXAMPLES OF SPECIFIC AGNOSIAS AND APRAXIAS Agnosia:Disorders of high-level sensory analysis = Difficulty in recognizing things. Apraxia:Disorders of high-level motor co-ordination and appropriateness = clumsiness for a particular task. Associated with lesions of the cerebellum or motor cortex.

7. Aphasia:Disorders in communicating using symbols involves the mental mechanism for forming concepts, for understanding symbols and making sentences. Examples of specific aphasias Name:Area of Difficulty DyarthriaArticulation AphoniaSpeaking DyslexiaReading

8. DysgraphiaWriting Broca’s (Expressive) aphasia Expression of communication Wernicke’s (sensory) aphasia Understanding communication Conduction aphasiaRepeating Nominal aphasiaRecalling names Global aphasiaAll aspects of communication AmusiaMusic AcalculiaArithmetic

9. Examples of Specific Agnosias and Apraxias: Names Area of Difficulty AstereognosiaTactile recognition Visual agnosiaVisual recognition Auditory agnosiaAuditory recognition Spatial agnosia Orientation, drawing, maps, etc. AnosognosiaAppreciation of body topography

10. Prosopagnosia Recognition of faces Motor apraxia Execution of skilled sequences Constructional apraxia Assembling components into a whole Ideational apraxia Formulation of plans of action

11. FRONTAL LOBE Damage lead to profound personality change, Mood changes (euphoria): childishness, making jokes and performs pranks. Lack of Drive and motivation, inability to plan, impaired judgment, poor social awareness. Perseveration of

12. speech & movements, pallilalia or repetition of phrases and sentences, low verbal fluency. Motor Area: -Lies posterior to frontal lobe -Body is inverted Damage - Contra lateral hemiparesis, +Grasp Reflex, urinary incontinence.

13. Posterior part of dominant frontal lobe > Apraxia of the face, motor aphasia, motor agraphia. Broca’s area (Broadman’s area 44 & 45). Posterior frontal cortex > Problems with verbal expression (poor articulation and sparse speech) = Expressive or Broca’s aphasia.

14. Temporal lobe damage Amnesia, personality disturbances, visual field and sensory deficits. dominant lobe > More symptoms and sign. Temporal lobe is the final destination for different sensory modalities including auditory, vestibular, gustatory and olfactory senses.

15. Bilateral medial temporal lobe lesions cause Amnesia. Intact immediate memory (digit span). Anterograde > Retrograde amnesia Personality change, e.g. depersonalization, emotional instability, aggression and antisocial behaviour. Psychosis, e.g. Temporal lobe epilepsy Visual field deficit (optic radiation) > contra lateral homonymous upper quardrant visual field defect.

16. Other changes Dominant lobe > sensory or receptive aphasia Posterior part of temporal lobe (commoner in non-dominant hemisphere) Alexia – inability to read Graphic - inability to write Hemisomatognosia – part of body felt absent. Prosopagnosia – inability to recognize faces Visuospatial problems

17. Wernicke’s auditory association area/superior temporal cortex > reduced verbal comprehension,reading and writing abilities. Speech – fluent but nonsensical = Jargon aphasia/wernicke’s or receptive aphasia. Kluver-bucy syndrome = Bilateral ablation of temporal lobes + destruction of uncus, amygdala and hippocampus.

18. Causes increased oral and sexual behaviours, placidity, loss of fear or anger, apathy, pet-like compliance. Seen in Pick’s disease, Alzheimer's dementia, arteriosclerosis, cerebral tumours, herpes simplex encephalitis. Parietal Lobe Complex tasks Integration of information, e.g. recognition, visuo spatial abilities and appreciation of environmental cues.

19. Parietal lobe syndrome consists of -Constructional apraxia -Visuospatial inattention -Topographical disorientation -Visual inattention -Cortical sensory loss (objects felt but not fully interpreted or discriminated). Dominant lobe – motor aphasia (anterior) - sensory aphasia (posterior)

20. Gerstmann’s syndrome - dominant parietal lobe> Dyscalculia, agraphia, finger agnosia, right-left disorientation. Non dominant: Anosognosia - Failure to recognize disable limb, Hemisomatognosia,Dressing apraxia (difficulty putting on clothes),Prosopagnosia.

21. Occipital Lobe Processes visual information Dominant lobe lesion Alexia, Agraphia, Colour agnosia, visual object agnosia. Non dominant lesion Visuospatial agnosia, prosopagnosia, metamorphosia (image distortion), complex visual hallucinations.

22. Occipital lobe syndrome = contra lateral homonymous hemianopla, scotomata and simultagnosia (inability to recognize complex pictures). The Cerebellum Gross anatomy 2 hemispheres and midline vermis. Functions = coordination of movement, maintenance of muscle tone and equilibrium

23. Archicerebellum = Inferior vermis > vestibular nuclei. Maintenance of body equilibrium. Lesion causes broad-based gait.Palleocerebellum = anterior lobe. Receive afferents from spinocerebellar tracts and sends efferents to vestibular and reticular nuclei. F x n = muscle tone and final control of movements. Lesions affect extension tone.

24. Neocerebellum = Posterior lobe and tonsil. It’s a relay for cortical information from pontine nuclei. Concerned with skilled voluntary movements. Cerebellar Dysfunction Receives information from eyes, ears, proprioceptors, brain stem, cortex and reticular formation. Integrates and relays information about movement smooth coordinated motor function.

25. Cerebellar dysfunction – Truncal ataxia and dysequilibrum. Reduced muscle tone and reflexes muscles tire easily. Poor coordination of movements dysdiadochokinesis, past pointing(dysmetria), intention tremor. Speech-slurred and jerky, explosive and intermittent. Nystagmus, gait is wide-based ataxia