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 Δs, 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.