Khanna Session 20 2024 PBC9102 Post Bacc Anatomy II Head & Neck.pdf

Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine Pre-medical Post-Baccalaureate Program BRAIN & NERVOUS SYSTEM - 5 DEEPESH KHANNA, MD, PH.D., MPH, MBA, MS, CPH LEARNING OBJECTIVES Name the structural components of the diencephalon  Describe the visual pathways  Descr...

Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine Pre-medical Post-Baccalaureate Program BRAIN & NERVOUS SYSTEM - 5 DEEPESH KHANNA, MD, PH.D., MPH, MBA, MS, CPH LEARNING OBJECTIVES Name the structural components of the diencephalon  Describe the visual pathways  Describe the components of the basal ganglia and its pathway  Diencephalon Components Gross Feature Hidden from the surface of the brain EXCEPT at inferior surface EXTENDS from: Anterior – Interventricular foramina (Monroe) Posterior – Cerebral aqueduct Boundaries: Superiorly: Corpus callosum Fornix Lateral ventricle Septum pellucidum Laterally: Caudate nucleus Internal nucleus Medially: 3rd ventricle – cavity of diencephalons, bordered bilaterally by the thalamus & hypothalamus Interthalamic adhesion Diencephalon MRI Hypothalalmus Thalamus THALAMUS  Large egg-shaped mass of gray matter  Forms major part of diencephalons  Situated on each side of the 3rd ventricle  Serves as a cell station to all main sensory systems. EXCEPT olfactory  Activities are closely related to that of cerebral cortex *damage to thalamus cause great loss of cerebral function  THALAMUS THALAMIC RADIATIONS Thalamic fibers project to the cerebral cortex Travel in internal capsule THALAMUS Nuclei Anterior Ventral posteromedial Ventral posterolateral Ventral anterior/lateral Mediodorsal Pulvinar Medial geniculate body Lateral geniculate body Intralaminar/midline THALAMUS ANTERIOR ANTERIOR PART  Contains anterior nucleus  Receives mamilothalamic tract from mammillary nuclei  Reciprocal connections with cingulated gyrus & hypothalamus  Function: Associated with the limbic system, emotional tone & mechanisms of recent memory THALAMUS VENTRAL POSTERIOR Ventral posterior: 3 subnuclei Ventral posterolateral – receives spinothalamic, spinal & medial lemnisci (inputs from libs & trunk) Ventral posteromedial – receives ascending trigeminal & taste pathways (input from anterior head) Ventral posteroinferior – receives vestibulothalamic fibers from vestibular nuclei *Projects to the sensory cortex – sensory nuclei THALAMUS MEDIAL PART Dorsomedial nucleus Reciprocal connections with prefrontal cortex of frontal lobe & hypothalamic nuclei o Plays a role in expression of affect, emotion & Behavior When destroyed, causes memory loss (Wernickes – Korsakoff syndrome) Midline nucleus Diffuse, small nuclei in the paraventricular area & inner thalamic adhesion Relay information for the consciousness system THALAMUS PULVINAR Input Visual, auditory, and other sensory pathways Output Parietotemporal-occipital association Function Orientation towardvisual, auditory, and other sensory stimuli THALAMUS MEDIAL GENICULATE BODY (MGB) Auditory relay nuclei Receives auditory input via Brachium of Inferior colliculus Projects to primary auditory cortex via auditory radiation THALAMUS LATERAL GENICULATE BODY (LGB) Input Retina/superior colliculus Output Primary visual cortex Function Relays visual input to cortex THALAMUS INTRALAMINAR/MIDLINE (IL/ML) Involved in arousal Reticular activating system THALAMIC NUCLEI RETICULAR ACTIVATING SYSTEM Cortex + + = Excitatory action + + + Non-specific thalamus + + + – = Inhibitory action; without considering specific thalamic nuclei ARAS (Ascending Reticular Activating System) + Stimuli of noradrenergic fibres of the brainstem + Visual stimuli – Stimuli of serotonergic fibres of the brainstem HYPOTHALAMUS NUCLEI HYPOTHALAMUS PARAVENTRICULAR AND SUPRAOPTIC PV Release of ADH and Oxytocin Regulation of: fluid balance (lesion: diabetes insipidus) Lactation Parturition SO HYPOTHALAMUS PREOPTIC AREA Regulation of: thermoregulation, sexual behavior (sexual dimorphism = differs in function between males and female) Lesions: loss of control of sexual behavior, amenorrhea, impotence POA HYPOTHALAMUS ANTERIOR Regulation: thermoregulation (cooling of the body),sleep Lesion: hyperthermia A HYPOTHALAMUS SUPRACHIASMATIC Regulation: circadian rhythms (direct input from the retina) Lesions: elimination of circadian rhythms SC HYPOTHALAMUS DORSOMEDIAL DM Regulation: physiological circadian rhythms (eating, drinking, energy consumption), ingestive behavior, cardiovascular responses to stress Lesion: overeating (hyperphagia), when food intake is restricted,rage outbursts may be provoked HYPOTHALAMUS VENTROMEDIAL Regulation: appetite and satiety, consumption, fear, energy thermoregulation Lesions: hyperphagia, obesity syndrome HYPOTHALAMUS POSTERIOR Regulation: thermoregulation (heating of the body) Lesion: hypothermia HYPOTHALAMUS MAMMILLARY BODIES Emotion Regulation: recollective memory Lesion: memory deficits, pathogenesis of Wernicke's Encephalopathy HYPOTHALAMUS LATERAL AREA Regulation: appetite and satiety, pain perception, thermoregulation, digestive function, blood pressure, sleep pattern Lesion: narcolepsy, motility disorders or functional gastrointestinal disorders, eating disorders (starvation, weight loss) HYPOTHALAMUS ARCUATE Control of anterior pituitary – releasing and inhibiting hormones Regulation: hormone secretion (prolactin) of the pituitary gland via mainly Dopamine and GHRH, regulation of appetite and body weight (via Neuropeptide Y) Lesion: galactorrhea, hyperphagia, obesity syndrome HYPOTHALAMUS INFLUENCE ON PITUITARY Adenohypophysis Neurohypophysis Epithalamus Components Pineal gland Habenular nuclei EPITHALAMUS FUNCTION OF PINEALGLAND Secretion of melatonin Regulation of circadian rhythm HABENULAR NUCLEI  Essential integrating center, and a region strongly implicated in neurological disorders and addiction  The habenular nuclei are located just anterior to the pineal gland and consist of a large lateral nucleus and a small medial nucleus  Both nuclei contribute axons to the habenulointerpeduncular tract (fasciculus retroflexus), which terminates in the midbrain interpeduncular nucleus  The stria medullaris thalami, which arches over the medial aspect of the dorsal thalamus near the midline, conveys input to both habenular nuclei SUBTHALAMUS FUNCTION subthalamus is located within the diencephalon, one of the major divisions of the prosencephalon (forebrain) Together, the diencephalon and the telencephalon, which is the cerebrum, comprise the forebrain Responsible for relaying information between regions of the brain and controlling many autonomic functions in the peripheral nervous system (PNS) Serves to connect the endocrine system with the nervous and limbic system primarily to regulate emotions and memories Although the subthalamus is a structure within the forebrain, it is made up of tissues that arise from the midbrain and is largely interconnected with the basal ganglia. Structural member of thebasal ganglia Lesion causes contralateral hemiballism SUBTHALAMUS FUNCTION Possible causes of lesion Vascular HIV infection Neoplasm Nonketotic hyperglycemia EYEBALL PASSAGE OF LIGHT RETINA MAJOR LAYERS AND OPTIC NERVE Pigment epithelium Photoreceptors Bipolar cells Ganglion cells Optic nerve RETINA PHOTORECEPTORS Rods Cones CONES FUNCTIONS  Bright light  Color vision (red, green, and blue cones)  High visual acuity  Loss causes legal blindness RODS FUNCTIONS Low light vision Poor visual acuity Achromatic vision Loss causes night blindness RETINA RETINALDETACHMENT Separation of neural retina from pigment epithelium Blood supply to photoreceptorcells is disrupted Shower of pepper or floaters arevisual sensations extravasated RBCs PUPILLARY LIGHT REFLEX NEURAL CIRCUITRY Pretectal area Right Light in left eye Ganglion retinal cells Optic nerve to pretectal area Bilateral innervation of EdingerWestphal nucleus Edinger-Westphal nucleus Left PUPILLARY LIGHTREFLEX NEURAL CIRCUITRY Pretectal area Right Parasympathetic fibers travel to ciliary ganglion Edinger-Westphal nucleus Thence, fibers innervate sphincter muscle Direct and consensual light reflexes Oculomotor nerve Ciliary ganglion Left ACCOMMODATION MECHANISM Edinger-Westphal nucleus Preganglionic parasympathetic fibers from Edinger-Westphal nucleus Conveyed in oculomotor nerve Synapse in ciliary ganglion Oculomotor nerve Ciliary ganglion ACCOMMODATION MECHANISM Edinger-Westphal nucleus Postganglionic parasympathetic fibers innervate ciliary muscle Ciliary muscle contracts decreasing tension on suspensory ligaments Lens increases its convexityfor near vision Oculomotor nerve Ciliary ganglion VISUAL PATHWAY RETINA TO PRIMARY VISUALCORTEX VISUAL PATHWAY RETINA TO PRIMARY VISUALCORTEX Temporal and nasal retina Temporal retina optic nerve fibers travel ipsilaterally into optic tract Nasal retina optic nerve fibers travel through optic chiasm into contralateral optic tract VISUAL PATHWAY RETINA TO PRIMARY VISUALCORTEX Most synapse in lateral geniculate body (LGB) Some project to superior colliculi, pretectal area, and suprachiasmatic nucleus LGB neurons travel in the optic radiations to the visual cortex in occiptal lobe Optic radiations LESIONS ENTIRE RIGHT OPTICNERVE Loss of vision in right eye(anopia) Causes Trauma Optic neuritis Lesion of right N. opticus (II) (blindness of right eye) LESIONS PARTIAL LESION OF LEFT OPTIC NERVE Loss of left temporal retina and blindness of left nasal visual field (left nasal hemianopsia) Causes Tumor Arterial dysfunction Partial lesion of left N. opticus(II) (blindness of the left nasal) visual fields and loss of the left temporal retina) LESIONS LATERAL PORTION OF RIGHT OPTIC NERVE AT OPTIC CHIASM Loss of right temporal retina and blindness of right nasal visual field (right nasal hemianopsia) Left upper temporal quadrantanopsia (partial effect on the left inferonasal fibers thathave crossed) Cause Aneuysmal compression by internal carotid artery Lesion in the lateral portion of the right N. opticus (II) at the level of the Chiasma opticum (nasal fibers from the right side have already crossed to the contralateral side) (right nasal hemianopsia and left temporal hemianopsia) LESIONS OPTIC CHIASM Bitemporal hemianopsia Causes Pituitary tumor Craniopharyngioma Median chiasma lesion (bitemporal hemianopsia) LESIONS RIGHT OPTIC TRACT Left homonymoushemianopsia Causes Tumor of temporal lobe Abscess of temporallobe Lesion of right Tractus opticus (left-sided homonymous hemianopsia) LESIONS RIGHT VISUALTRACT Lesions of the upper optic radiations Causes:parietal or occipital lobe tumor Lesion of the right upper optic radiations located anterior in the temporal lobe (left homonymous inferior quadrant anopsia) LESIONS RIGHT VISUALTRACT Lesions of the lower optic radiations ( loop) Causes: temporal or occipital lobe tumor Lesion of the right visual tract located anterior in the temporal lobe (left homonymous superior quadrant anopsia) LESIONS ENTIRE VISUALTRACT Left homonymoushemianopsia Causes Tumors Arterial dysfunction Trauma Lesion of the complete right visual tract (leftsided homonymous hemianopsia) VISUAL FIELD DEFECTS BASAL GANGLIA BASAL GANGLIA MAJOR STRUCTURES Striatum Globus pallidus Substantia nigra Subthalamic nucleus (notshown) WHERE ARE THE BASAL GANGLIA? BG dysfxn Slow, inefficient actions, rigidity, bradykinesia, unwanted movement CONNECTIONS  BG has multiple connections with other parts of CNS- cerebral cortex, cerebellum, thalamus,reticular formation, mid brain.  They are imp. Centres of coordination, in control of automatic associated movements.  Corpus striatum(C+P) is responsible for initiation and inhibition of gross intentional body movements that are unconsciously performed in normal person.  Also provide muscle tone – so that exact movements can be performed,hand workrequiring coordinated effort of entire arm & trunk for hand to be able to perform. Connections Caudate nucleus Putamen Globus pallidus – receive input output leaves Connections Connections of striatum – Caudate nucleus & putamen – input – Receive afferent cerebral cortex, intralaminar thalamic nuclei, subs nigra – Efferent – globus pallidus, subs nigra Connections of globus pallidus – 2 segments – GPi & GPe – GPi& subs nigra – output – Receive afferent – striatum, subthalamic nucleus – Efferent GPe – subthalamic N GPi– thalamus (VA,VL,CM) – motor areas Thus, the direct & indirect pathways have opposing actions. An increase in either one of these pathways – leads to imbalance in motor control. It influences increase/ decrease in motor output of cortex. Neurons of SN (pc)- project to striatum (3rd circuit)Dopamine is the neurotransmitter. This has an excitatory effect on Direct and Inhibitory action on indirect pathway. – Both actions facilitate activity in C.Cortex. – This circuit is imp. Functionally. Direct Pathway Striatum ➔ (-) GPi, SNr Indirect Striatum ➔ (-) GPe ➔ (-) STN ➔ (+) GPi Effect on BG output GPi, SNr inhibited GPi stimulated Effect on Thalamus Stimulated Inhibited Effect on movement Initiated Inhibited Malfxning Parkinson’s Huntington’s bradykinesia Chorea Basal Ganglia Connections Circuit of connections –cortex to basal ganglia to thalamus to cortex –Helps to program automatic movement sequences (walking and arm swinging or laughing at a joke) Output from basal ganglia to reticular formation –reduces muscle tone –damage produces rigidity of Parkinson’s disease CLINICAL CORRELATIONS PARKINSON‘S DISEASE Cerebal cortex Loss of dopaminergic neurons Thalamus Direct pathway not excited Indirect pathway is no longer inhibited Net effect is that indirect pathway inhibits motor neurons Motor execution is diminished Striatum Subthalamic nucleus Substantia nigra Globus pallidus internal segment; external segment CLINICAL CORRELATIONS PARKINSON‘S DISEASE Symptoms Structural changes and causes Bradykinesis or akinesia Depigmentation of substantia nigra Rigidity Lewy bodies Resting tremor of hands and fingers Difficulty initiating movements Movements are abnormally slow Decreased facial expression Causes include genetics, environment, certain medications, MPTP, and vascular insult CLINICAL CORRELATIONS HUNTINGTON‘S DISEASE – DIRECTPATHWAY Thalamus Loss of GABAergic striatal neurons in the direct pathway Loss of inhibitory influence on globus pallidus, internal segment Thalamus is inhibited Cortex is understimulated Cerebal cortex Striatum Subthalamic nucleus Substantia nigra Globus pallidus internal segment; external segment CLINICAL CORRELATIONS HUNTINGTON‘S DISEASE – INDIRECTPATHWAY Cerebal cortex Loss of GABAergic striatal neurons in the indirect pathway Loss of inhibitory influence of indirect pathway Motor cortex is over excited Motor programs executed withno control by patient Thalamus Striatum Subthalamic nucleus Substantia nigra Globus pallidus internal segment; external segment CLINICAL CORRELATIONS HUNTINGTON‘S DISEASE Symptoms Structural changes and causes Chorea Loss of GABAergic, medium size, spiny neurons from striatum Athetosis Ventricular enlargement Personality changes Genetic cause – autosomal dominant Dementia Excessive CGA repeats