Frontal lobe functions: Mvmt: Mediated by 1° & supplementary motor areas. Voluntary mvmt of eyes to opposite side: Mediated by frontal eye fields; attention, planning, judgment, insight, abstract thinking; language: See below.

Lesions involving the frontal lobe & clinical manifestations: Orbitofrontal synd: Disinhibition, impulsive behavior. Frontal convexity synd: Apathetic, angry/aggressive behavior. There may be associated disturbances in mvmt. Medial frontal synd: Mutism, gait disturbances, & bladder incontinence. Massive frontal lobe lesion: Akinetic, apathetic, & abulic state. Broca area: Inf frontal region in areas 44 & 45; resultant expressive aphasia characterized by nonfluent speech w/rel intact comprehension & impaired repetition, reading, & writing.

Parietal lobe functions: Sensation: Somatosensory area in postcentral gyrus.

Attention: Typically nondominant → contralat hemispatial neglect, anosognosia.

Lesions involving the parietal lobe & clinical manifestations: Gerstmann synd: Lesion in dominant, angular gyrus → acalculia, alexia, finger agnosia, L-R confusion. Balint synd: Bilat parietooccipital lesions; often due to watershed infarcts between PCA & MCA territories. Sx incl optic ataxia, ocular apraxia, visual inattention, simultagnosia.

Temporal lobe functions: Recognition of stimuli. Hearing: Mediated by 1° auditory areas in transv temporal gyrus & 2° auditory areas in sup temporal gyrus. Memory: Mediated by hippocampus. Language: See below.

Lesions involving the temporal lobe & clinical manifestations: Prosopagnosia: Bilat or nondominant occipital temporal lesion → inability to identify or recognize faces. Kluver-Bucy synd: Bilat lesions of the medial temporal lobes or amygdala → hyperorality, hypersexuality, changes in emotional behavior. Wernicke aphasia: Receptive language disturbance w/nonsensical fluent speech w/poor comprehension & repetition.

Occipital lobe functions: Vision (calcarine cortex): Lesions may cause blindness, vision loss, or visual agnosia.

Lesions involving the occipital lobe & clinical manifestations: Anton synd: Bilat parietooccipital lesions → unaware of blindness. Preserved pupillary light reaction. Palinopsia: Persistence of visual image for several minutes despite gazing at another scene. Often 2° to occipitotemporal dz or during recovery from cortical blindness. Alexia w/o agraphia: Dom occipital lobe & splenium of corpus callosum, accompanied by R homonymous hemianopia & color naming deficits.

Lateralization of cerebral hemispheres: Right hemisphere: Spatial & constructional skills, nonvisuospatial perception, emotional tone of speech. Left hemisphere: Language, analytic & mathematic skills, reasoning.

Major white matter tracts connecting hemispheres: Corpus callosum, anterior commissure.

Components: Caudate, putamen, external & internal globus pallidus, subthalamic nucleus, substantia nigra pars compacta (SNPc) & pars reticulata. Striatum = caudate + putamen, lentiform nucleus = putamen + globus pallidus.

Basal ganglia pathways: Control of posture & mvmt. Involves complex excitatory & inhibitory networks, which influence mvmt. Inputs to basal ganglia: From cortex, thalamus, substantia nigra, raphe nuclei. Outputs from basal ganglia: To globus pallidus, substantia nigra, thalamus, sup colliculus. Two pathways through the basal ganglia: direct & indirect pathway. Net effect of direct pathway is excitatory to stimulate mvmt, & net effect of indirect pathway is to inhibit mvmt. Damage to basal ganglia may also result in cognitive deficits, incl difficulty w/learning, particularly involv procedural memory, abulia, & ↓ executive function. Agitation, aphasia, neglect, obsessive-compulsive d/os have also been described w/basal ganglia lesions. Huntington dz: Loss of neurons projecting from striatum to globus pallidus externus → loss of inhibitory effect of indirect pathway.

Influence of the SNPc: Modulate activity of caudate & putamen (striatum). Two types of dopaminergic receptors in striatum: D1 & D2. D1: Excitatory to direct pathway. D2: Inhibitory to indirect pathway. Net effect of D1 & D2 activity is excitatory or to decrease inhibitory influence of basal ganglia. In Parkinson dz, there is loss of dopaminergic neurons of SNPc.

Lesions involving the basal ganglia & clinical manifestations: Subthalamic nucleus: Contralat hemiballismus. Caudate nucleus: Contralat choreoathetosis. Globus pallidus: Contralat hemidystonia, hemiparkinsonism, tremor. Substantia nigra: Parkinsonism. Unilat basal ganglia: Falling to contralat side & slow mvmts.

Thalamus is relay & integrative center connecting multiple areas of brain, including cortex, basal ganglia, hypothalamus, cerebellum, & brainstem.

Thalamic nuclei: Anterior nucleus: Memory. Projects to the cingulate gyrus. Receives connections from mammillary bodies via mammillothalamic tracts. Anterior nucleus or dorsomedial nucleus of thalamus may be affected in Wernicke-Korsakoff synd. Dorsomedial: Emotions, sleep-wake cycle, executive function. Receives input from prefrontal cortex & limbic structures. Major thalamic relay for info traveling to frontal association area. Ventral anterior: Motor control. Receives input from globus pallidus & projects to thalamus & frontal cortex. Ventral lateral: Motor control. Receives motor input from cerebellum & basal ganglia & projects to motor, premotor, & supplementary motor cortex. Ventral posterior medial & lateral: Relays sensory info from face & body, respectively, to primary somatosensory cortex. Medial geniculate: Relays auditory info from inf colliculus to transverse temporal (Heschl) gyrus. Lateral geniculate: Relays visual info from visual pathway to calcarine cortex. Pulvinar: Modulate occipitotemporoparietal cortical attention/visual processing. Reticular: Relays info between thalamic nuclei.

Vascular supply of the thalamus: Tuberothalamic artery: Arises from PComm. Paramedian artery: Branch of basilar or PCA. Posterior choroidal artery: Branch of P2 segment of PCA. Inferolateral artery (aka thalamogeniculate artery): From P2 segment of PCA.

Lesions involving the thalamus & clinical manifestations: Dejerine-Roussy synd: Thalamic pain synd w/hemisensory painful sensation. Korsakoff dementia: Degeneration of dorsomedial & anterior nuclei of thalamus, mammillothalamic tracts, mammillary bodies due to thiamine deficiency → memory loss, confabulation. Lesions in thalamus cause a significant variety of deficits, depend on location, include hemisensory loss, hemiparesis, abnormal mvmts, behavior &Dgr;s, akinetic mutism, somnolence, changes in mood, apathy, memory disturbances, neglect, deficits in ocular motility, small reactive pupils (diencephalic) visual field deficits, & language difficulty/aphasia.

Integrates sensory info & sends outputs to the cerebral cortex, brainstem, & spinal cord to coordinate mvmt. Lesions result in ataxia/irreg uncoordinated mvmts. Composed of flocculonodular lobe, vermis, & two hemispheres. Flocculonodular lesions → nystagmus, imbalance; vermis lesions → truncal ataxia; hemisphere lesions → limb ataxia. Ataxia is typically ipsi to the lesion. Cerebellar lesions may also result in ↓ intellectual function & cerebellar cognitive affective synd, characterized by ↓ executive function, difficulty w/visuospatial ability, flattened affect, inappropriate behavior, dysprosody, agrammatism.

Cerebellar anatomy: Cerebellar cortex: Three layers: molecular, Purkinje cell, granule cell. Deep cerebellar nuclei: Outputs from cerebellar cortex travel through deep nuclei to regulate upper motor neurons in cerebral cortex, brainstem, & spinal cord. Cerebellar nuclei from lateral to medial are dentate, emboliform, globose, & fastigial nuclei. Cerebellar peduncles: Connect cerebellum to brainstem. Sup: Efferent pathway. Deep cerebellar nuclei send efferents in the superior cerebellar peduncles to synapse in thalamus; thalamocortical projections complete the cerebellar-cerebral feedback circuit. Middle: Afferent pathway. Fibers from cortex & sup colliculus project to cerebellum via pons. Inf: Afferent & efferent. Efferents project to vestibular nuclei & reticular formation & afferent info from vestibular nuclei, spinal cord, & brainstem tegmentum.

Vascular supply to cerebellum: Sup cerebellar artery (SCA): sup portion. Anterior inf cerebellar artery (AICA): middle peduncles, middle ant hemispheres. Posterior inf cerebellar artery (PICA): inf portion.

I. Olfactory nerve: Smell. May be damaged due to head injury, tumors, neurodegenerative dz. Foster-Kennedy synd: Tumor/mass lesion compressing olfactory bulb & optic nerve causing ipsi anosmia, optic atrophy, & contralat papilledema.

II. Optic nerve: Vision; afferent pupillary light reflex.

III. Oculomotor nerve: Motor: Innervates sup, medial, & inf rectus, inf oblique, levator palpebrae superioris muscles. Autonomic: Efferent pupillary light reflex; lens accommodation.

INO (internuclear ophthalmoplegia): Due to medial longitudinal fasciculus (MLF) lesions; ipsi adduction paresis w/contralat abducting nystagmus.

WEBINO (wall-eyed bilat INO): Due to midbrain lesion involving both medial recti & both MLFs. Common in MS.

One & half synd: MLF + PPRF or MLF + sixth nuclear lesion causing ipsi adduction paresis w/gaze deviation to ipsi side, w/only mvmt contralat abducting nystagmus.

Horner synd: Classic triad: ptosis, miosis, anhidrosis. Other possible findings: “Upside down” ptosis from sympathetic denervation of lower eyelid retractor, heterochromia iridis (diff in eye color b/w two eyes) in congenital lesions, & apparent enophthalmos.