This document provides information on the anatomy and physiology of the visual system. It describes the structures involved in vision, including the eye, optic nerve, optic chiasm, and visual cortex. Key points covered include the layers of the retina, blood supply to the optic nerve head, pathways of the visual system from the retina to the brain, and tests used to evaluate visual acuity and visual fields.
The visual pathway begins in the retina and passes through the optic nerves, optic chiasm, optic tracts, lateral geniculate nucleus, optic radiations, and terminates in the occipital lobe. Lesions along this pathway can cause various visual field defects including hemianopias and quadrantanopias depending on the location of the lesion. Lesions in the optic nerve cause blindness on the affected side while lesions in the optic chiasm or tracts cause incongruous homonymous hemianopias. Lesions of the optic radiations or visual cortex cause congruous homonymous defects.
This document summarizes the functional anatomy of the cerebral hemispheres. It describes the six layers of the cerebral cortex and areas related to somatosensory, motor, visual, auditory, and olfactory functions. It discusses association areas including the parietooccipitotemporal area, prefrontal cortex, Wernicke's area, and angular gyrus. It also briefly mentions control of eye movements, face recognition, speech processing, and functions of the non-dominant hemisphere.
The third cranial nerve (oculomotor nerve) originates in the midbrain. It contains motor fibers that innervate four of the six extraocular muscles as well as the levator palpebrae superioris and the intraocular muscles that control the pupil and lens. The nerve exits the midbrain and travels through the cavernous sinus before dividing into superior and inferior branches in the orbit. The inferior branch provides motor input to three extraocular muscles and also carries preganglionic parasympathetic fibers to the ciliary ganglion which controls pupil constriction and accommodation.
The document discusses the anatomy and clinical presentations of the third cranial nerve (oculomotor nerve). It begins by describing the origin and course of the nerve, including its nuclei in the midbrain and pathways through the brainstem and cavernous sinus. It then discusses the individual branches and functions of the nerve in innervating the extraocular muscles and parasympathetic fibers to the eye. The summary concludes by noting that damage to the third cranial nerve can cause a total third nerve palsy presenting with ptosis, external eye movement limitations, pupil dilation and loss of accommodation.
This document discusses cranial nerves III, IV, and VI. It provides details on:
1. The functional components, origin nuclei, course, and functions of CN III, including its motor and parasympathetic roles.
2. The unique features and course of CN IV.
3. The origin, course, and role in lateral eye movement of CN VI.
4. Clinical signs that result from damage to different parts of these cranial nerves, such as diplopia and ptosis.
This document discusses accommodation, or the ability of the eye to focus on near objects. It defines accommodation and describes the three adjustments made: convergence of the eyeballs, constriction of the pupil, and an increase in the anterior curvature of the lens. The mechanism of accommodation involves the ciliary muscle contracting to relax the suspensory ligaments and allow the lens to become more spherical for focusing on near objects. The pathway for the accommodation reflex involves visual signals traveling from the retina to the visual cortex and frontal lobe, where efferent signals are sent to the ciliary muscle, sphincter pupillae, and medial rectus to enact the adjustments for accommodation. Presbyopia is described as the age-related loss
The abducens nerve originates in the pons and contains motor neurons that innervate the lateral rectus muscle, allowing for eye movement outward. It exits the brainstem and travels through the cavernous sinus before entering the orbit through the superior orbital fissure to innervate the lateral rectus. Pathologies of the abducens nerve can occur at the nuclear, central, cisternal, petrous, cavernous, or orbital segments and result in lateral rectus palsy and limitations in abduction of the eye. Common causes include pontine hemorrhage, MS, meningiomas, and traumatic injuries.
The visual pathway begins in the retina and passes through the optic nerves, optic chiasm, optic tracts, lateral geniculate nucleus, optic radiations, and terminates in the occipital lobe. Lesions along this pathway can cause various visual field defects including hemianopias and quadrantanopias depending on the location of the lesion. Lesions in the optic nerve cause blindness on the affected side while lesions in the optic chiasm or tracts cause incongruous homonymous hemianopias. Lesions of the optic radiations or visual cortex cause congruous homonymous defects.
This document summarizes the functional anatomy of the cerebral hemispheres. It describes the six layers of the cerebral cortex and areas related to somatosensory, motor, visual, auditory, and olfactory functions. It discusses association areas including the parietooccipitotemporal area, prefrontal cortex, Wernicke's area, and angular gyrus. It also briefly mentions control of eye movements, face recognition, speech processing, and functions of the non-dominant hemisphere.
The third cranial nerve (oculomotor nerve) originates in the midbrain. It contains motor fibers that innervate four of the six extraocular muscles as well as the levator palpebrae superioris and the intraocular muscles that control the pupil and lens. The nerve exits the midbrain and travels through the cavernous sinus before dividing into superior and inferior branches in the orbit. The inferior branch provides motor input to three extraocular muscles and also carries preganglionic parasympathetic fibers to the ciliary ganglion which controls pupil constriction and accommodation.
The document discusses the anatomy and clinical presentations of the third cranial nerve (oculomotor nerve). It begins by describing the origin and course of the nerve, including its nuclei in the midbrain and pathways through the brainstem and cavernous sinus. It then discusses the individual branches and functions of the nerve in innervating the extraocular muscles and parasympathetic fibers to the eye. The summary concludes by noting that damage to the third cranial nerve can cause a total third nerve palsy presenting with ptosis, external eye movement limitations, pupil dilation and loss of accommodation.
This document discusses cranial nerves III, IV, and VI. It provides details on:
1. The functional components, origin nuclei, course, and functions of CN III, including its motor and parasympathetic roles.
2. The unique features and course of CN IV.
3. The origin, course, and role in lateral eye movement of CN VI.
4. Clinical signs that result from damage to different parts of these cranial nerves, such as diplopia and ptosis.
This document discusses accommodation, or the ability of the eye to focus on near objects. It defines accommodation and describes the three adjustments made: convergence of the eyeballs, constriction of the pupil, and an increase in the anterior curvature of the lens. The mechanism of accommodation involves the ciliary muscle contracting to relax the suspensory ligaments and allow the lens to become more spherical for focusing on near objects. The pathway for the accommodation reflex involves visual signals traveling from the retina to the visual cortex and frontal lobe, where efferent signals are sent to the ciliary muscle, sphincter pupillae, and medial rectus to enact the adjustments for accommodation. Presbyopia is described as the age-related loss
The abducens nerve originates in the pons and contains motor neurons that innervate the lateral rectus muscle, allowing for eye movement outward. It exits the brainstem and travels through the cavernous sinus before entering the orbit through the superior orbital fissure to innervate the lateral rectus. Pathologies of the abducens nerve can occur at the nuclear, central, cisternal, petrous, cavernous, or orbital segments and result in lateral rectus palsy and limitations in abduction of the eye. Common causes include pontine hemorrhage, MS, meningiomas, and traumatic injuries.
This document provides an overview of the anatomy and clinical assessment of the optic nerve in 3 paragraphs:
1) It describes the anatomy of the optic nerve, including its origin from the ganglion cells and path from the optic disc to the optic chiasm. It is composed of over 1 million axons and is divided into intraocular, intraorbital, intracanalicular, and intracranial portions.
2) Clinical assessment of the optic nerve involves testing visual acuity, color vision, visual fields, and the pupillary light reflex. Signs of optic nerve pathology include an afferent pupillary defect.
3) Different pathologies like papilledema, optic neuritis, and optic
The internal capsule is a compact bundle of fibers that connects different regions of the brain. It has three parts - the anterior limb, genu, and posterior limb. It contains association fibers connecting different cortical regions, projection fibers connecting the cortex to other gray matter structures, and commissural fibers connecting the left and right hemispheres. The internal capsule receives its blood supply from the lateral striate branches of the middle cerebral artery, medial striate branches of the anterior cerebral artery, and the anterior choroidal artery from the internal carotid artery.
Cranial nerves III, IV, and VI are described. Cranial nerve III is the oculomotor nerve, with motor nuclei in the midbrain. It innervates extraocular muscles and the iris and ciliary body. Cranial nerve IV is the trochlear nerve, with its nucleus in the midbrain. It crosses and innervates the superior oblique muscle. Cranial nerve VI is the abducent nerve, with its nucleus in the pons. It supplies the lateral rectus muscle. Palsies of each nerve are also described.
This document summarizes the anatomy and physiology of eye movements. It describes the six extraocular muscles that control eye movement and their innervation by three cranial nerves. It discusses the different types of eye movements including saccades, smooth pursuit, optokinetic nystagmus, vergence, and vestibulo-ocular movements. It also outlines the brain structures involved in motor control of eye movements, including the frontal eye fields, superior colliculus, brainstem gaze centers, and their connections.
The light reflex causes pupillary constriction when light enters the eyes. There are two types of light reflex - direct and consensual. The pathway involves signals traveling from the retina to the pretectal nuclei and then to the Edinger-Westphal nucleus which triggers the parasympathetic nervous system to constrict the pupil. The accommodation reflex controls focusing of the lens and involves signals from the retina and pretectal nuclei to the Edinger-Westphal nucleus which triggers the ciliary muscle via parasympathetic pathways. Both reflexes are controlled by a balance of parasympathetic and sympathetic signals to regulate pupil size and lens focusing.
The document provides an overview of eye movements, including:
1) The different types of eye movements (saccades, smooth pursuit, vergence, vestibular-ocular reflex, optokinetic reflex) and the neural pathways that control each type.
2) Saccades involve rapid eye movements to fixate on objects of interest, while smooth pursuit keeps a moving target on the fovea. Vergence aligns the eyes for near and far vision. The vestibular-ocular reflex and optokinetic reflex stabilize gaze during head movements.
3) Precise control of the extraocular muscles allows for the different eye movement types, each with specific neural circuits and functions for optimal vision. Measurements
The document discusses the oculomotor nerve, including its anatomy, causes of third nerve palsy, and how to localize lesions. It describes the nuclei of origin and pathways of the nerve. Causes of third nerve palsy are discussed for the nuclear, midbrain fascicular, subarachnoid fascicular, cavernous sinus fascicular, and orbital fascicular portions. Signs that help localize lesions are described, such as contralateral findings that indicate a nuclear lesion versus isolated ipsilateral findings for a fascicular lesion. Evaluation of extraocular movements, pupil, and other cranial nerves is covered to help determine the location of a lesion affecting the third nerve.
This document discusses the anatomy and functions of the corpus callosum. It describes the corpus callosum as the wide bundle of neural fibers beneath the cortex that connects the left and right cerebral hemispheres. It summarizes that the corpus callosum is divided into five regions - the splenium, body, genu, rostrum, and isthmus. It also briefly discusses the blood supply, development, and functions of the different regions of the corpus callosum.
1) The visual pathway consists of the optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations, and visual cortex.
2) The optic nerve carries visual information from the retina to the optic chiasm. At the chiasm, fibers from the nasal retina cross to the opposite side while temporal fibers remain uncrossed.
3) Lesions in different parts of the visual pathway cause characteristic visual field defects, such as optic nerve lesions causing blindness, chiasmal lesions causing bitemporal hemianopia, and cortical lesions causing homonymous hemianopia.
Pupillary light reflex (PLR) : that controls the diameter of the pupil, in
response to the intensity of light that falls on the retinal ganglion cells of
the retina in the back of the eye.
- Light reflex
- Corneal reflex.
-Accommodation reflex:
Argyll Robertson pupils
Horner's syndrome:
Holmes–Adie syndrome
Horner's syndrome and Internuclear ophthalmoplegiaAnkit Raiyani
1. The document describes a case of a 26-year-old male presenting with progressive weakness in his right upper limb over 5 years and difficulty walking due to tightness in his right lower limb for 3 months. On examination, he showed signs of Horner's syndrome and LMN weakness in his right upper limb with UMN involvement in his right lower limb.
2. Imaging revealed basilar invagination and syringohydromyelia extending from C2-D9. He was diagnosed with a CV junction anomaly (basilar invagination) with dorsal syringohydromyelia.
3. The document then discusses Horner's syndrome, its localization, and
The optic nerve has four parts - intraocular, intraorbital, intracanalicular, and intracranial. It carries signals from the retina to the brain. The second order neurons are the retinal ganglion cells whose axons form the optic nerve. The optic chiasm allows fibers from the nasal retina to cross to the opposite side. The optic tracts relay signals from the optic chiasm to the lateral geniculate bodies. The optic radiations then carry signals from the LGBs to the visual cortex in the occipital lobe where visual perception occurs. Lesions in different parts of the visual pathway cause specific visual field defects.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
Anatomy of optic nerve and its clinical significancePabita Dhungel
This document discusses the anatomy and clinical significance of the optic nerve. It begins with a brief overview of the embryology and development of the optic nerve, from the formation of the optic vesicle and stalk in the early weeks of gestation through myelination and vascularization later in development. Next, it describes the anatomy of the optic nerve in detail at each stage from the intraocular portion to the visual cortex, including structures like the optic disc, chiasm, tract, lateral geniculate body, and optic radiation. The document concludes with a discussion of the clinical significance of understanding optic nerve anatomy, highlighting conditions like disc edema, congenital anomalies, vascular diseases, and how lesions at different points can cause different visual field defects.
This document summarizes key details about the 3rd (oculomotor), 4th (trochlear), and 6th (abducent) cranial nerves. It describes the nuclei, course, branches, and functions of each nerve. The oculomotor nerve supplies muscles that control eye movement and pupil constriction. The trochlear nerve solely innervates the superior oblique muscle. The abducent nerve solely innervates the lateral rectus muscle. Diagrams and references are also provided for additional information.
The reticular formation is a network of neurons located in the brainstem that performs several important functions. It receives sensory information from the spinal cord and senses arousal levels. The reticular formation contains nuclei that are involved in motor control, sleep-wake cycles, autonomic functions, and modulating pain. It has ascending and descending pathways that connect to the thalamus and cerebral cortex and help regulate states of consciousness like sleep and wakefulness.
The document discusses the basal ganglia, which are a group of subcortical gray matter structures in the cerebrum that include the corpus striatum, amygdala, and claustrum. It describes the main components and connections of the basal ganglia, including the striatum, globus pallidus, substantia nigra, and subthalamic nucleus. The basal ganglia are involved in coordinating movement through connections with the cerebral cortex, thalamus, and brainstem. Disorders like Parkinson's disease can result from basal ganglia dysfunction and cause issues like tremors, rigidity, and bradykinesia.
El documento resume la anatomía, fisiología, etiología y tratamiento de los trastornos olfatorios. Describe las cuatro vías quimiosensoriales intranasales, incluido el sistema olfatorio principal responsable del sentido del olfato. Explica las causas más comunes de hiposmia y anosmia, como traumatismos craneales, infecciones virales agudas de las vías respiratorias superiores e rinosinusitis crónica. También cubre las evaluaciones y opciones de tratamiento para los trastornos olfatorios
Mx guideline for post stroke rehablitationNeurologyKota
This document provides guidelines for stroke rehabilitation. It discusses that stroke affects nearly 800,000 people in the US each year, with most receiving rehabilitation after hospitalization. The aim is to provide best practices for rehabilitative care. It recommends assessment by rehabilitation experts and discusses various levels of post-acute care like inpatient rehabilitation facilities and skilled nursing facilities. Effective rehabilitation requires a coordinated team and communication is paramount.
This document provides an overview of the anatomy and clinical assessment of the optic nerve in 3 paragraphs:
1) It describes the anatomy of the optic nerve, including its origin from the ganglion cells and path from the optic disc to the optic chiasm. It is composed of over 1 million axons and is divided into intraocular, intraorbital, intracanalicular, and intracranial portions.
2) Clinical assessment of the optic nerve involves testing visual acuity, color vision, visual fields, and the pupillary light reflex. Signs of optic nerve pathology include an afferent pupillary defect.
3) Different pathologies like papilledema, optic neuritis, and optic
The internal capsule is a compact bundle of fibers that connects different regions of the brain. It has three parts - the anterior limb, genu, and posterior limb. It contains association fibers connecting different cortical regions, projection fibers connecting the cortex to other gray matter structures, and commissural fibers connecting the left and right hemispheres. The internal capsule receives its blood supply from the lateral striate branches of the middle cerebral artery, medial striate branches of the anterior cerebral artery, and the anterior choroidal artery from the internal carotid artery.
Cranial nerves III, IV, and VI are described. Cranial nerve III is the oculomotor nerve, with motor nuclei in the midbrain. It innervates extraocular muscles and the iris and ciliary body. Cranial nerve IV is the trochlear nerve, with its nucleus in the midbrain. It crosses and innervates the superior oblique muscle. Cranial nerve VI is the abducent nerve, with its nucleus in the pons. It supplies the lateral rectus muscle. Palsies of each nerve are also described.
This document summarizes the anatomy and physiology of eye movements. It describes the six extraocular muscles that control eye movement and their innervation by three cranial nerves. It discusses the different types of eye movements including saccades, smooth pursuit, optokinetic nystagmus, vergence, and vestibulo-ocular movements. It also outlines the brain structures involved in motor control of eye movements, including the frontal eye fields, superior colliculus, brainstem gaze centers, and their connections.
The light reflex causes pupillary constriction when light enters the eyes. There are two types of light reflex - direct and consensual. The pathway involves signals traveling from the retina to the pretectal nuclei and then to the Edinger-Westphal nucleus which triggers the parasympathetic nervous system to constrict the pupil. The accommodation reflex controls focusing of the lens and involves signals from the retina and pretectal nuclei to the Edinger-Westphal nucleus which triggers the ciliary muscle via parasympathetic pathways. Both reflexes are controlled by a balance of parasympathetic and sympathetic signals to regulate pupil size and lens focusing.
The document provides an overview of eye movements, including:
1) The different types of eye movements (saccades, smooth pursuit, vergence, vestibular-ocular reflex, optokinetic reflex) and the neural pathways that control each type.
2) Saccades involve rapid eye movements to fixate on objects of interest, while smooth pursuit keeps a moving target on the fovea. Vergence aligns the eyes for near and far vision. The vestibular-ocular reflex and optokinetic reflex stabilize gaze during head movements.
3) Precise control of the extraocular muscles allows for the different eye movement types, each with specific neural circuits and functions for optimal vision. Measurements
The document discusses the oculomotor nerve, including its anatomy, causes of third nerve palsy, and how to localize lesions. It describes the nuclei of origin and pathways of the nerve. Causes of third nerve palsy are discussed for the nuclear, midbrain fascicular, subarachnoid fascicular, cavernous sinus fascicular, and orbital fascicular portions. Signs that help localize lesions are described, such as contralateral findings that indicate a nuclear lesion versus isolated ipsilateral findings for a fascicular lesion. Evaluation of extraocular movements, pupil, and other cranial nerves is covered to help determine the location of a lesion affecting the third nerve.
This document discusses the anatomy and functions of the corpus callosum. It describes the corpus callosum as the wide bundle of neural fibers beneath the cortex that connects the left and right cerebral hemispheres. It summarizes that the corpus callosum is divided into five regions - the splenium, body, genu, rostrum, and isthmus. It also briefly discusses the blood supply, development, and functions of the different regions of the corpus callosum.
1) The visual pathway consists of the optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations, and visual cortex.
2) The optic nerve carries visual information from the retina to the optic chiasm. At the chiasm, fibers from the nasal retina cross to the opposite side while temporal fibers remain uncrossed.
3) Lesions in different parts of the visual pathway cause characteristic visual field defects, such as optic nerve lesions causing blindness, chiasmal lesions causing bitemporal hemianopia, and cortical lesions causing homonymous hemianopia.
Pupillary light reflex (PLR) : that controls the diameter of the pupil, in
response to the intensity of light that falls on the retinal ganglion cells of
the retina in the back of the eye.
- Light reflex
- Corneal reflex.
-Accommodation reflex:
Argyll Robertson pupils
Horner's syndrome:
Holmes–Adie syndrome
Horner's syndrome and Internuclear ophthalmoplegiaAnkit Raiyani
1. The document describes a case of a 26-year-old male presenting with progressive weakness in his right upper limb over 5 years and difficulty walking due to tightness in his right lower limb for 3 months. On examination, he showed signs of Horner's syndrome and LMN weakness in his right upper limb with UMN involvement in his right lower limb.
2. Imaging revealed basilar invagination and syringohydromyelia extending from C2-D9. He was diagnosed with a CV junction anomaly (basilar invagination) with dorsal syringohydromyelia.
3. The document then discusses Horner's syndrome, its localization, and
The optic nerve has four parts - intraocular, intraorbital, intracanalicular, and intracranial. It carries signals from the retina to the brain. The second order neurons are the retinal ganglion cells whose axons form the optic nerve. The optic chiasm allows fibers from the nasal retina to cross to the opposite side. The optic tracts relay signals from the optic chiasm to the lateral geniculate bodies. The optic radiations then carry signals from the LGBs to the visual cortex in the occipital lobe where visual perception occurs. Lesions in different parts of the visual pathway cause specific visual field defects.
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
Anatomy of optic nerve and its clinical significancePabita Dhungel
This document discusses the anatomy and clinical significance of the optic nerve. It begins with a brief overview of the embryology and development of the optic nerve, from the formation of the optic vesicle and stalk in the early weeks of gestation through myelination and vascularization later in development. Next, it describes the anatomy of the optic nerve in detail at each stage from the intraocular portion to the visual cortex, including structures like the optic disc, chiasm, tract, lateral geniculate body, and optic radiation. The document concludes with a discussion of the clinical significance of understanding optic nerve anatomy, highlighting conditions like disc edema, congenital anomalies, vascular diseases, and how lesions at different points can cause different visual field defects.
This document summarizes key details about the 3rd (oculomotor), 4th (trochlear), and 6th (abducent) cranial nerves. It describes the nuclei, course, branches, and functions of each nerve. The oculomotor nerve supplies muscles that control eye movement and pupil constriction. The trochlear nerve solely innervates the superior oblique muscle. The abducent nerve solely innervates the lateral rectus muscle. Diagrams and references are also provided for additional information.
The reticular formation is a network of neurons located in the brainstem that performs several important functions. It receives sensory information from the spinal cord and senses arousal levels. The reticular formation contains nuclei that are involved in motor control, sleep-wake cycles, autonomic functions, and modulating pain. It has ascending and descending pathways that connect to the thalamus and cerebral cortex and help regulate states of consciousness like sleep and wakefulness.
The document discusses the basal ganglia, which are a group of subcortical gray matter structures in the cerebrum that include the corpus striatum, amygdala, and claustrum. It describes the main components and connections of the basal ganglia, including the striatum, globus pallidus, substantia nigra, and subthalamic nucleus. The basal ganglia are involved in coordinating movement through connections with the cerebral cortex, thalamus, and brainstem. Disorders like Parkinson's disease can result from basal ganglia dysfunction and cause issues like tremors, rigidity, and bradykinesia.
El documento resume la anatomía, fisiología, etiología y tratamiento de los trastornos olfatorios. Describe las cuatro vías quimiosensoriales intranasales, incluido el sistema olfatorio principal responsable del sentido del olfato. Explica las causas más comunes de hiposmia y anosmia, como traumatismos craneales, infecciones virales agudas de las vías respiratorias superiores e rinosinusitis crónica. También cubre las evaluaciones y opciones de tratamiento para los trastornos olfatorios
Mx guideline for post stroke rehablitationNeurologyKota
This document provides guidelines for stroke rehabilitation. It discusses that stroke affects nearly 800,000 people in the US each year, with most receiving rehabilitation after hospitalization. The aim is to provide best practices for rehabilitative care. It recommends assessment by rehabilitation experts and discusses various levels of post-acute care like inpatient rehabilitation facilities and skilled nursing facilities. Effective rehabilitation requires a coordinated team and communication is paramount.
This document summarizes the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2) trial, which aimed to determine if rapidly lowering systolic blood pressure to ≤140 mm Hg (intensive treatment) versus ≤180 mm Hg (standard treatment) in patients with intracerebral hemorrhage treated within 4.5 hours of symptom onset reduces death and disability. The trial randomized patients to 24 hours of intravenous nicardipine to achieve the assigned blood pressure target. The primary outcome was death or disability (modified Rankin score 4-6) at 3 months. Secondary outcomes included hematoma expansion and quality of life measures.
The document discusses cranial nerves XI and XII. CN XI is the spinal accessory nerve which has a cranial and spinal portion. The cranial portion innervates muscles of the larynx while the spinal portion innervates the sternocleidomastoid and trapezius muscles. CN XII is the hypoglossal nerve which solely innervates the muscles of the tongue. Clinical examination of both nerves involves assessing strength and movement of their respective muscles. Lesions can occur at supranuclear, nuclear or infranuclear levels and cause varying patterns of weakness depending on the location.
1. The document summarizes current stroke intervention strategies, including intravenous fibrinolysis (tPA), endovascular interventions like intra-arterial fibrinolysis and mechanical thrombectomy, and decompressive craniotomy.
2. Intravenous tPA is recommended within 3 hours and may be considered within 3-4.5 hours for select patients. Several trials have demonstrated the benefits of intravenous tPA.
3. Intra-arterial fibrinolysis and mechanical thrombectomy are beneficial options for carefully selected patients not eligible for intravenous tPA or who have failed intravenous tPA. Recent trials show improved outcomes with newer mechanical thrombectomy devices compared to older technologies.
This document discusses motor rehabilitation after acute stroke. It notes that the majority of neurological recovery occurs within the first 3 months after stroke, but can continue for up to 1 year. Motor rehabilitation aims to reacquire lost movement skills through meaningful, repetitive, intensive, task-specific practice in an enriched environment. Current treatment methods discussed include constraint-induced movement therapy, treadmill training, robotic training, electrical stimulation, noninvasive brain stimulation, mirror therapy, and selective serotonin reuptake inhibitors.
Brain death current concepts and legal issues in indiaNeurologyKota
This document discusses the history and criteria for determining brain death. It begins by outlining the historical definitions of death from the 1960s onwards, which evolved from cardiopulmonary criteria to brain-based criteria with the development of life-support technologies. The document then examines the anatomical basis of brainstem death and causes that can lead to it. It provides details on the clinical evaluation process for determining brain death in both adults and children based on guidelines from the US and UK. The document also discusses legal aspects of brain death certification in India according to the Transplantation of Human Organs Act.
This document provides detailed information about the anatomy, physiology, and clinical examination of the vestibulocochlear nerve (CN VIII), which has both auditory and vestibular components. It describes the structures of the inner ear, including the cochlea, semicircular canals, utricle, and saccule. It also outlines the central pathways of the auditory and vestibular systems and clinical tests used to evaluate hearing and balance function, such as audiometry, auditory evoked potentials, and tuning fork tests.
The document discusses the glossopharyngeal (CN IX) and vagus (CN X) nerves. It covers their anatomy, functions, and clinical assessment. The glossopharyngeal nerve innervates the pharynx and posterior tongue. The vagus nerve is the longest cranial nerve, innervating muscles of the pharynx and larynx, and the heart and gastrointestinal tract via parasympathetic fibers. Clinical examination focuses on motor function of soft palate, larynx, and reflexes. Lesions are localized based on involved structures and associated deficits in other cranial nerves.
Carotid artery stenting – an update on atheroscleroticNeurologyKota
Carotid artery stenting is an alternative to carotid endarterectomy for treating carotid artery stenosis caused by atherosclerosis. The document provides recommendations for treatment of asymptomatic and symptomatic carotid stenosis. It summarizes data from trials comparing outcomes of carotid endarterectomy and stenting to medical management. The risks and benefits of carotid endarterectomy and stenting are discussed, along with indications, contraindications, procedural details, complications, and long-term outcomes of the procedures. Guidelines recommend carotid endarterectomy or stenting only when the risk of perioperative stroke and death is low (<6%).
This document provides an overview of neuromyelitis optica spectrum disorders (NMOSD). It discusses the epidemiology, clinical features, diagnostic criteria, investigations, neuroimaging findings, and treatments for NMOSD. Key points include that NMOSD predominantly affects the optic nerves and spinal cord, is strongly associated with antibodies against the aquaporin-4 protein, and treatments involve high-dose steroids, plasma exchange, or intravenous immunoglobulins for acute exacerbations. The diagnostic criteria were revised in 2015 to incorporate aquaporin-4 antibody testing and distinguish NMOSD from multiple sclerosis.
The facial nerve is a mixed nerve that controls muscles of facial expression and sensation. It has motor, sensory, and parasympathetic components. The motor component innervates muscles of the face and head. The sensory component conveys taste from the tongue and sensation from the ear. The parasympathetic component regulates salivary and tear glands. Examination of the facial nerve tests motor function by asking the patient to move facial muscles, sensory function by testing taste and ear sensation, and secretory function by measuring tear and saliva levels.
1. Platelets play an important role in both normal hemostasis and pathological thromboses like myocardial infarction and stroke. Antiplatelet drugs are commonly used to prevent strokes.
2. Aspirin is recommended for both primary and secondary stroke prevention. Clopidogrel and dipyridamole are also options for secondary prevention. Combination aspirin/dipyridamole may be better than aspirin alone.
3. Newer antiplatelets like ticagrelor inhibit the P2Y12 receptor more effectively than clopidogrel, but trials found no clear benefit over aspirin for acute stroke. Combining aspirin and clopidogrel long-term increases bleeding risk without
This document discusses cardioembolic stroke, which occurs when heart issues cause materials to enter the brain's blood vessels. Common causes include atrial fibrillation, heart failure, and mechanical heart valves. Diagnosis involves echocardiography and monitoring for embolic signals. Treatment depends on the specific heart condition but often includes anticoagulants to prevent clots. Anticoagulation reduces stroke risk from atrial fibrillation by 60-90% compared to placebo. Managing cardioembolic stroke risk requires identifying the underlying heart condition and addressing it with medications, surgery, or lifestyle changes.
This document provides information on primary headache disorders, with a focus on migraine. It discusses the structures in the head that are sensitive to pain, and classifies headaches as either primary (having no underlying cause) or secondary (having an identifiable structural or metabolic cause). The primary headaches are further classified, with detailed descriptions and diagnostic criteria provided for migraine without aura, migraine with aura, and tension-type headache. Pathophysiology, epidemiology, triggers, management approaches including acute and preventive therapies are summarized for migraine. Botulinum toxin, triptans, ergot alkaloids, and other medication options are outlined for migraine treatment.
The document provides information on the functional neuroanatomy of the spinal cord. It discusses the development, gross anatomy, cross-sectional anatomy, tracts (ascending and descending), blood supply, and lesions of the spinal cord. Key points include that the spinal cord extends from the cranial border of C1 to L1-L2 in adults and has a cervical and lumbar enlargement. It consists of 31 pairs of spinal nerves and has gray matter in an H-shape surrounded by white matter. Major ascending tracts include the posterior column and spinothalamic tracts, while major descending tracts are the corticospinal, rubrospinal, and reticulospinal tracts. Complete transverse spinal cord injury
The document discusses the parietal lobe of the brain. The parietal lobe is located towards the top and middle of the brain. It is involved in processing sensory information like touch, pressure, temperature, and pain. The document also likely discusses how the parietal lobe is evaluated through neurological exams and imaging tests.
El documento describe la estructura y funcionamiento del sistema olfativo. El sistema olfativo está compuesto del epitelio olfatorio, bulbo olfatorio, tracto olfatorio y centros olfatorios del cerebro. Las moléculas olorosas estimulan las células receptoras en el epitelio nasal, generando impulsos nerviosos que viajan al bulbo olfatorio y centros cerebrales para la interpretación de olores.
The optic nerve carries visual information from the retina to the brain. It passes through the optic canal and forms the optic chiasm, where fibers from the nasal retina cross over. The optic tracts continue into the lateral geniculate bodies and optic radiations to the visual cortex. Damage to different parts of this visual pathway causes characteristic visual field defects, including hemianopias and quadrantanopias. The optic nerve receives blood supply from the ophthalmic and central retinal arteries.
The conjunctiva is the mucous membrane that lines the inner surface of the eyelids and covers the anterior surface of the sclera and cornea. It has three layers - an epithelial layer, adenoid layer, and fibrous layer. The conjunctiva receives its blood supply from the marginal arterial arcade, peripheral arterial arcade, and anterior ciliary arteries. It drains into the venous plexus of the eyelids and then into the superior and inferior ophthalmic veins. Lymphatic drainage is to the preauricular and submandibular lymph nodes. Pterygium is a wing-shaped growth of conjunctiva that extends onto the cornea, caused by exposure to sun and dust, and is
The facial nerve is a mixed nerve that is predominantly motor. It innervates the muscles of facial expression and the scalp, ear, and neck. It has motor, sensory, and parasympathetic secretomotor functions. The facial nerve exits the brainstem and travels through the internal acoustic meatus, facial canal, and stylomastoid foramen before branching in the parotid gland. It gives off several branches including the chorda tympani, nerve to stapedius, and branches to neck muscles.
The trigeminal nerve is the largest cranial nerve and is a mixed nerve containing both sensory and motor fibers. It has three major divisions - the ophthalmic, maxillary, and mandibular nerves. The ophthalmic nerve innervates the face above the eyes. The maxillary nerve innervates the midface, and the mandibular nerve innervates the lower face and jaw muscles. The trigeminal ganglion contains the cell bodies of the pseudounipolar neurons whose axons make up the trigeminal nerve. The trigeminal nuclei in the brainstem are involved in relaying sensory information from the trigeminal nerve.
Anatomy of visual pathway and its lesions.Ruchi Pherwani
1) The visual pathway begins with photoreceptors in the retina which transmit visual information via the optic nerve and optic chiasm to the lateral geniculate nucleus. It then continues via the optic radiations to the primary visual cortex.
2) Lesions along the visual pathway can cause different types of visual field defects, including complete blindness from optic nerve lesions, bitemporal hemianopia from chiasmal lesions, and homonymous hemianopia from lesions of the optic tract or beyond.
3) The document discusses the anatomy and blood supply of structures in the visual pathway like the optic nerve, chiasm, tract, lateral geniculate nucleus and visual cortex. It also describes various causes and characteristics
This document provides an overview of the trigeminal nerve (CN V), which is the largest of the cranial nerves and contains both sensory and motor fibers. It has three major divisions - ophthalmic, maxillary, and mandibular. The trigeminal ganglion contains the cell bodies of the pseudounipolar sensory neurons. The nerve has sensory and motor nuclei in the brainstem and connects to various ganglia. The three divisions and their branches innervate different regions of the face and head. Clinical implications of lesions or damage to parts of the trigeminal nerve are also discussed.
This document provides information on the cranial nerves:
1. It discusses the embryology, classification, types, components, functions and clinical relevance of the 12 cranial nerves.
2. Specific details are provided on the first 3 cranial nerves - olfactory, optic and oculomotor. For each nerve, the summary includes its component, function, origin, exit point from the brain, and some key clinical points.
3. The embryology section describes the embryonic origin of the cranial nerves into 3 groups from different developmental periods, and notes that most cranial and spinal sensory ganglia arise from neural crest cells.
The optic nerve originates in the retina and passes through the optic canal to the optic chiasm. It carries axons from retinal ganglion cells that terminate in the lateral geniculate nucleus and optic radiation, ultimately projecting to the visual cortex. The oculomotor nerve originates in the midbrain and supplies motor innervation to four extraocular muscles and the superior tarsal muscle as well as parasympathetic fibers to the iris and ciliary body.
Surgical anatomy of cranial nerves pallavpallavkedia
The document provides an overview of the 12 pairs of cranial nerves:
- It describes the names, numbers and basic functions of each cranial nerve.
- It discusses the nuclei, pathways and branches of several key nerves - the trigeminal, facial, glossopharyngeal and vagus nerves - in more detail.
- It explains that cranial nerves have both sensory and motor components, and lists their functional roles like proprioception, vision, taste, etc.
The visual pathway begins in the retina and passes through the optic nerves, optic chiasm, and optic tracts to synapse in the lateral geniculate nucleus (LGN). From the LGN, fibers pass through the temporal and parietal lobes to terminate in the occipital lobes in the visual cortex. Lesions in different parts of the visual pathway can cause specific visual field defects, such as lesions of the optic nerve causing complete blindness in the affected eye.
The visual pathway begins with light entering the retina and transmitting signals along the optic nerve. The two optic nerves meet at the optic chiasm before projecting to the lateral geniculate nucleus. Signals then travel along the optic radiations to the primary visual cortex in the occipital lobe. The visual cortex integrates this information and transmits it to additional visual processing areas for functions like object recognition and motion detection. Disruptions to the visual pathway can result in visual field defects depending on the location of injury or disease.
The trigeminal nerve is a mixed nerve that is the largest of the cranial nerves. It has both sensory and motor functions. Sensory branches provide sensation to the face and motor branches innervate the muscles of mastication. The trigeminal nerve has three major divisions - ophthalmic, maxillary, and mandibular nerves. These divisions branch further to innervate specific regions of the face. The trigeminal ganglion contains the cell bodies of pseudounipolar neurons that relay sensory information from the face to the brainstem trigeminal nuclei.
The optic nerve develops from the embryonic optic stalk and connects the optic vesicle to the forebrain. It begins forming in the 8th week of embryogenesis and myelination is completed shortly after birth. The optic nerve has four parts - intraocular, intraorbital, intracanalicular, and intracranial. It transmits visual information from the retina to the brain and is supplied by branches from the ophthalmic artery and central retinal artery.
The document discusses the trigeminal nerve (cranial nerve V) in three sentences: It describes the trigeminal nerve as the largest cranial nerve, a mixed nerve with both motor and sensory components. It originates from the trigeminal ganglion and divides into three main branches - the ophthalmic, maxillary, and mandibular nerves - which innervate the face and associated structures. The document provides detailed information on the embryology, nuclei, course and branches of the trigeminal nerve.
The retina is the innermost layer of the eye that converts light into neural signals. It contains several layers of tissue and cell types that carry out this visual transduction process. The outermost layer contains pigmented cells, followed by photoreceptor cells (rods and cones), bipolar and ganglion cells that transmit signals to the brain. Within the retina, the macula provides high-acuity central vision and the optic disc is where retinal ganglion cell axons exit as the optic nerve. The retina receives its blood supply from the central retinal artery and precise vascular architecture is important for normal visual function.
Optic Nerve Applied Anatomy, Clinical Evaluation and Approaches.pptxAgraj Mishra
This document summarizes the anatomy and clinical evaluation of the optic nerve and visual pathways. It describes the four portions of the optic nerve from the eye to the optic chiasm. The intraocular portion contains the optic disc. The intraorbital portion is surrounded by fat and muscles in the orbit. The intracanalicular portion travels through the optic canal. The intracranial portion extends to the optic chiasm. Clinical evaluation of the visual pathways includes testing visual acuity, color vision, visual fields, pupillary response, and fundus examination. Visual field defects can localize lesions along the visual pathways.
This document summarizes the anatomy and arrangement of fibers in the visual pathway, from the retina through the optic nerve, optic chiasm, optic tract, lateral geniculate body, optic radiations, and visual cortex. It also describes common lesions that can occur at different points along the visual pathway and their associated clinical presentations, such as optic nerve lesions causing complete blindness in the affected eye.
Anatomy of external and middle ear by dr. faisal rahmanFaisalRahman153
This includes anatomy of external and middle ear with their clinical co relations. Embryology is also discussed here. Pinna, External auditory canal, Tympanic membrane, Middle ear Cleft, Mastoid and Auditory tube topics are included.
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
emergence of autoimmune neuropathies and role of nodal and paranodal regions in their pathophysiology.
Peripheral neuropathies are traditionally categorized into demyelinating or axonal.
dysfunction at nodal/paranodal region key for better understanding of patients with immune mediated neuropathies.
antibodies targeting node and paranode of myelinated nerves have been increasingly detected in patients with immune mediated neuropathies.
have clinical phenotype similar common inflammatory neuropathies like Guillain Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
they respond poorly to conventional first line immunotherapies like IVIG
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptxNeurologyKota
The document discusses neurological scales used to assess consciousness. It describes the Glasgow Coma Scale (GCS), which evaluates best eye opening, best verbal response, and best motor response on a scale of 3 to 15. The Full Outline of UnResponsiveness (FOUR) score is also discussed, which measures eye responses, motor responses, brainstem reflexes, and respiratory patterns on a scale of 0 to 16. The FOUR score is presented as having advantages over the GCS in certain clinical situations. A new scale, the FIVE score, is also mentioned which builds upon the FOUR score.
LOCALISATION OF LESION CAUSING COMA.pptxNeurologyKota
1) The document discusses signs that can help localize lesions causing coma, including abnormalities in respiratory patterns, pupil size and response, eye movements, and corneal and limb reflexes.
2) Specific lesions like thalamic or brainstem hemorrhages can cause signs like wrong-way eyes or downward eye deviation.
3) Examining responses like the oculocephalic reflex or corneal reflex can help determine if the brainstem is intact and localize lesions.
Dr. Bharat Bhushan is a professor of medicine and interventional neurologist at Government Medical College in Kota, Rajasthan, India. He has over 18 years of experience and qualifications including MBBS, MD, DM in Neurology, and FICP. He has published over 35 research papers and contributed to several medical research projects. The document discusses the concept of a "treadmill for the brain" to improve cognitive fitness through a balanced routine of exercise, sleep, and diet in order to stimulate and exercise the brain. It emphasizes coordinating the adaptation of organs like the gut, muscles and brain for overall health and quality of life.
Remote robotic thrombectomy is a promising technique to expand access to endovascular thrombectomy for acute ischemic stroke. The Corindus robotic system allows neurointerventionists to perform thrombectomy procedures remotely using robotic arms. This could allow thrombectomy-capable centers to treat patients from further distances. Early studies show robotic thrombectomy is technically feasible and reduces radiation exposure compared to manual procedures. However, further research is still needed as robotic systems require additional training and have limitations such as lack of haptic feedback. Overall, remote robotic thrombectomy may help more patients receive timely endovascular treatment for stroke.
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptxNeurologyKota
The document discusses autonomic function tests which are used to evaluate autonomic nervous system disorders. It describes various cardiovascular, sudomotor and pupillary reflex tests to assess different aspects of autonomic function. Cardiovascular tests include postural challenge tests, Valsalva maneuver, deep breathing test and isometric handgrip test. Sudomotor tests include quantitative sudomotor axon reflex test and thermoregulatory sweat test. The tests help diagnose autonomic dysfunction, evaluate its severity and distribution. Management involves identifying and treating the underlying cause, along with medications and lifestyle changes to alleviate symptoms like orthostatic hypotension.
Transcranial Doppler (TCD) ultrasonography is a noninvasive technique used to evaluate cerebral blood flow velocities. It was originally introduced in 1982 to detect vasospasm in subarachnoid hemorrhage. TCD is now used for a variety of purposes including detection of stenosis, occlusion, emboli, shunts, and vasospasm. It provides diagnostic information for conditions such as stroke, sickle cell disease, brain death, and arteriovenous malformations. TCD utilizes Doppler effect to measure blood flow velocities in basal cerebral arteries which provides data to assess hemodynamics and diagnose various cerebrovascular diseases.
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptxNeurologyKota
1) The document discusses intracerebral hemorrhage (ICH) in young adults aged 18-50 years.
2) Risk factors for ICH in this age group include hypertension, smoking, alcohol, medications like anticoagulants and cocaine use.
3) Common causes of ICH in young adults are structural abnormalities like arteriovenous malformations, aneurysms, and cavernomas. Other causes include hypertension, coagulopathies, vasculitis and reversible cerebral vasoconstriction syndrome.
A 42-year-old male patient was admitted with repeated dizziness and right-sided weakness for over 3 months. Imaging showed a linear filling defect in the proximal left internal carotid artery, revealing over 90% stenosis and delayed blood flow. The patient underwent carotid endarterectomy and was discharged on medical therapy. Three months later, the patient experienced recurrent symptoms. Carotid web was considered a potential cause given the patient's age and lack of atherosclerosis history. Intervention may be a safe and effective option for symptomatic carotid web in addition to medical management, with recurrent risk up to 26.8% with medical management alone.
This document discusses immune reconstitution inflammatory syndrome (IRIS) in patients with HIV. It provides background on IRIS, defines the two types (paradoxical and unmasked), and lists risk factors. It then discusses the pathology of IRIS and various pathogens that can cause central nervous system IRIS, including PML, cryptococcal meningitis, VZV, CMV, and mycobacteria. Specific details are provided on the clinical manifestations and imaging findings of PML-IRIS and cryptococcal meningitis-IRIS.
Epileptic encephalopathies are a group of epileptic disorders that cause cognitive and behavioral impairments beyond what would be expected from seizures alone. They typically begin early in life and are characterized by frequent seizures and abnormal EEG patterns. Common types include early myoclonic encephalopathy, Ohtahara syndrome, West syndrome, Dravet syndrome, and Lennox-Gastaut syndrome. These disorders can cause developmental delays, intellectual disabilities, and in some cases early death. Treatment aims to control seizures, though many types are highly treatment resistant.
This presentation briefs out the approach of dementia assessment in line with consideration of recent advances. Now the pattern of assessment has evolved towards examining each individual domain rather than lobar assessment.
Young onset dementia (YOD) refers to dementia with an onset before age 65. About 5% of all dementias are YOD. Common causes include Alzheimer's disease, vascular dementia, frontotemporal lobar degeneration, and dementia with Lewy bodies. A thorough evaluation includes medical history, physical and neurological exams, imaging like MRI and PET, and may involve genetic testing. Management focuses on treating underlying causes if possible, addressing behavioral and psychiatric symptoms, and providing social support. Prognosis varies by the specific cause but on average YOD results in 10-15 years shorter life expectancy than later onset dementia.
This document provides an overview of encephalopathy, including:
- Encephalopathy is defined as an altered mental state caused by diffuse brain dysfunction. Common symptoms include confusion, memory loss, and personality changes.
- There are many potential causes of encephalopathy including metabolic disturbances, toxins, infections, liver failure, inflammation, drugs, demyelination, and lack of oxygen to the brain.
- EEG is often abnormal in encephalopathy, with features including triphasic waves and diffuse slowing correlating to severity of symptoms and impairment of consciousness.
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER NeurologyKota
1. Functional neurological disorder is characterized by neurological symptoms that cannot be fully explained by organic disease. It is associated with psychological stressors and symptoms are not intentionally produced.
2. Associated psychological features include gaining secondary benefits from illness and showing indifference to serious symptoms.
3. Common clinical features are functional limb weakness, seizures, facial spasms, and clenched fists or inverted feet. Diagnosis is made by a neurologist based on inconsistent or non-organic physical signs.
Hyperthermic syndrome in ICU and their management.pptxNeurologyKota
Based on the information provided, this patient is likely experiencing malignant hyperthermia (MH). Key signs include:
- Muscle rigidity developing post-operatively
- Increasing tachycardia, tachypnea, and rising temperature shortly after being admitted to PACU
- Recent exposure to inhalational anesthetic triggers for MH like halothane during surgery
The immediate steps in management should be:
1. Discontinue any triggering anesthetic agents
2. Administer dantrolene sodium 2-3 mg/kg IV to reduce calcium release and muscle rigidity
3. Initiate cooling measures and monitor for signs of multiple organ dysfunction as temperature rises further
Prompt diagnosis and
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
This presentation contains information about the various Entrapment syndromes of Lower limb in descending order of topography. It also contains information about etiology, clinical features and management of each of these entrapment syndromes with special emphasis on electrodiagnostic confirmation.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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2. Anatomy
First order neurons-bipolar sensory cells in
olfactory epithelium (superior nasal concha,
upper nasal septum, roof of the nose)
Tiny knobs on cilia-sites of chemosensory
signal transduction.
Specific odorants stimulate specific receptor
cells.
Central processes of olfactory neurons-
unmyelinated axons
3. Form approximately 20 branches on each
side-olfactory nerves.
Penetrate cribriform plate of ethmoid bone,
acquire a sheath of meninges, synapse in
olfactory bulbs.
Basal cells in olfactory epithelium can
regenerate.
Within olfactory bulbs, synapse on dendrites
of mitral and tufted cells in olfactory
glomeruli.
4. Second order neurons-axons of mitral cells
Course posteriorly through olfactory tracts in
olfactory grooves beneath frontal lobes
Divide into medial and lateral olfactory striae.
Medial olfactory stria terminate on medial
surface of cerebral hemisphere in
paraolfactory area, subcallosal gyrus and
inferior part of cingulate gyrus.
Lateral olfactory stria terminate in uncus,
anterior hippocampal gyrus, piriform cortex,
entorhinal cortex, and amygdaloid nucleus
5.
6. History
◦ Unilateral or bilateral
◦ Altered taste
◦ Past head injury;
◦ Smoking
◦ Recent upper-respiratory infection
◦ Systemic illness
◦ Nutrition
◦ Exposure to toxins, medications or illicit drugs.
7. Before evaluating smell- nasal passages are
open.
Smell is tested using nonirritating stimuli.
Avoid irritating substances-stimulate trigeminal
nerve
Examine each nostril separately while occluding
other with eyes closed
Perception more important than accurate
identification
University of Pennsylvania smell identification
test (UPSIT) and Connecticut chemosensory test..
8. Term Definition
Anosmia No sense of smell
Hyposmia decrease in the sense of smell
Hyperosmia overly acute sense of smell
Dysosmia Impairment or defect in the sense of smell
Parosmia Perversion or distortion of smell
Phantosmia Perception of an odor that is not real
Presbyosmia Decrease in the sense of smell due to aging
Cacosmia Inappropriately disagreeable odors
Coprosmia fecal scent
Olfactory agnosia Inability to identify or interpret detected odors
10. 5 cm in length
Extends from ganglion cell layer of retina to
optic chiasm.
Divided into
◦ Intraocular:1mm
◦ Intraorbital:25mm
◦ Intracanalicular:9mm
◦ Intracranial:12-16mm
Organized into 400 to 600 fascicles
separated by connective tissue septae.
Intraorbital portion-surrounded by fat
11. Macula-point of central fixation and greatest
visual acuity and color perception.
Small shallow depression temporal to disc
Fovea (L. “pit”) centralis-depression that lies
in center of macula.
Foveola-tinier depression in center of fovea.
Point of most acute vision as overlying retinal
layers are pushed aside
Optical center of eye
Macula-central 15° of vision
12. Optic disc, or papilla-ophthalmoscopically
visible tip of intraocular portion of optic
nerve.
1.5 mm by 1.8 mm vertical ellipse
Pink to yellowish-white disc.
No receptor cells
Does not respond to visual stimuli-
physiologic blind spot
Macula-forms center of retina
Macular fixation point-center of clinical visual
field (VF).
13. Blood supply to optic nerve head-circle of
Zinn-Haller,
Composed of 2 often not connected
semicircles of short posterior ciliary arteries.
NAION- drop in perfusion pressure in short
posterior ciliary arteries is culprit.
Segmental disc edema corresponding to the
semicircle compromised
14.
15. Retinal ganglion cell axons form retinal nerve
fiber layer (NFL)
Exit through lamina cribrosa (L. “sieve”)
Myelinated at posterior end of optic nerve
head
Myelin-CNS myelin
1.2 million fibers in each optic nerve;
16. Intracranial dura at posterior globe fuses with
Tenon's capsule
Adherent in optic foramen to periosteum.
Pia and arachnoid fuses with sclera where nerve
terminates
Intracranial meninges extend forward along optic
nerves for a variable distance, forming vaginal
sheaths.
Variations in vaginal sheath anatomy
Intervaginal space-small subdural and a larger
sub-arachnoid space
17. Intraorbital portion-lies within muscle cone.
Before entering optic canal, surrounded by
annulus of Zinn formed by origins of rectus
muscles.
Superior and medial recti partially originate from
sheath of optic nerve.
Length of intraorbital portion greater than length
of orbit
Blood supply-pial vascular plexus and branches
of ophthalmic artery; distally central retinal artery
also contributes intraneural branches.
18. Intracanalicular portion-into cranium through
optic canal
Orbital opening of canal-vertical ellipse;
intracranial end-horizontal ellipse
1.2 cm in length, and located in lesser wing
of sphenoid bone.
Dural sheath fused to periosteum-
immobilizing nerve.
Medial wall of canal-thinnest part
Blood supply-ophthalmic artery.
19. Intracranial portion-travel 12-16 mm to optic
chiasm.
Ophthalmic arteries above, internal carotid
arteries superiorly and medially, and anterior
cerebral arteries that cross over optic nerves
and are connected by anterior communicating
artery.
Posterior to cavernous sinus-join together to
form optic chiasm;
Blood supply-branches of internal carotid and
ophthalmic arteries.
20.
21. Optic chiasm-lies about 10 mm above
pituitary gland, separated by suprasellar
cistern.
Fibers from temporal retina continue directly
back: nasal retina decussate to enter opposite
optic tract.
Fibers from inferior nasal quadrant loop
forward into opposite optic nerve for a short
distance before turning back again, forming
Wilbrand's knee.
22. Some of upper nasal fibers loop back briefly
into ipsilateral optic tract before decussation.
In chiasm, fibers from upper retinal
quadrants lie superior: lower quadrants
inferior
Inferior nasal fibers decussate anteriorly and
inferiorly: superior nasal fibers cross
posteriorly and superiorly
Macular fibers-decussate as a group,
forming a miniature chiasm within chiasm,
primarily posterior superior portion.
23.
24. Cavernous sinuses and carotid siphons lie just
lateral to chiasm
Anterior cerebral and anterior communicating
arteries front and above
Third ventricle and hypothalamus behind and
above.
Sella tursica and sphenoid sinus lie below.
Ophthalmic artery-same dural sheath through
canal and orbit.
8 mm to 12 mm posterior to globe, artery enters
nerve and runs along its center to optic disc-
central retinal artery
Divides at disc head into superior and inferior
branches.
25. 55% of axons of optic tract- contralateral
nasal retina; 45% ipsilateral temporal retina
80% visual afferents and 20% pupillary
afferents.
Fibers from upper retina-medial position,
inferior retina lateral.
PMB-dorsal and lateral position,
Majority of fibers terminate at LGB.
Six neuronal layers in the LGB
Ipsilateral temporal hemiretina synapse in
layers 2, 3, and 5;contralateral nasal
hemiretina synapse in layers 1, 4, and 6.
26. Geniculocalcarine tract, or optic radiations
Terminate in calcarine cortex of occipital lobe
Pass through retrolenticular portion of
internal capsule and then fan out.
Upper retinal fibers upper, and lower retinal
fibers lower in optic radiation
27. Inferior retinal fibers arch anteriorly into
temporal lobe, sweeping forward and laterally
above inferior horn of ventricle then laterally,
down, backward.
Meyer's loop (loop of Meyer and
Archambault).
Fibers from superior retina run directly back
in deep parietal lobe in external sagittal
stratum, lateral to posterior horn of lateral
ventricle
28. Primary visual cortex (calcarine area or striate
cortex)-Brodmann's area 17 on medial
surface of occipital lobe.
Lower retinal fibers- lower lip of calcarine
fissure (lingual gyrus)
Upper retinal fibers-upper lip of the calcarine
fissure (cuneus).
Most peripheral parts of retina-most
anteriorly in calcarine cortex
Macular -More posterior its calcarine
representation.
29.
30. Visual acuity
◦ Minimum visibility-smallest area that can be
perceived
◦ Minimum separability-ability to recognize the
separateness of two close points or lines
◦ Snellen chart for distance and near card for near
◦ In infants and children- blink to threat or bright
light, following movements, pupillary reactions
◦ Acuity- line where more than half of characters are
accurately read
31. Distance from test chart, 20 or 6-numerator, and
distance at which smallest type read by patient should
be seen by a person with normal acuity-denominator.
RAPD or Marcus gunn pupil
◦ Swinging light test
◦ Light shone into a pupil and then quickly switched
to other one.
◦ If one pupil dilates, even slightly, when light is
switched-RAPD present in that eye.
32.
33. Near vision
Jaeger chart
Newspaper want-ad text is approximately J-
0, regular newsprint J-6, and newspaper
headlines J-17.
Counts fingers (CF), hand motion (HM), light
perception (LP), or no light perception (NLP).
Count fingers at 5 ft-20/800.
34. Non organic visual loss
1. Ask to sign
2. Schmidt-Rimpler test- look toward his hand
3. Join the forefingers
4. Menace test
5. Ask patient look into a large mirror that can
be held and moved. Tilting and moving the
mirror will elicit OKN responses
35. Color Vision; Day and Night Vision
Color plates or pseudoisochromatic plates
(Ishihara, Hardy-Ritter-Rand )
In neurologic disease, red perception usually
lost first
Compare brightness or intensity of examining
light in one eye versus other
36. Visual field
Normal VF- 90 degrees to 100 degrees
temporally, about 60 degrees nasally, 50
degrees to 60 degrees superiorly, and 60
degrees to 75 degrees inferiorly
Examination most accurate in an individual
who is alert and cooperative and maintain
fixation.
Confrontation test
Moving pen light
Menace reflex
37. Formal visual field testing
Central fields-tangent screen
Peripheral fields-perimetry
Notation numerator-test object size and
denominator-distance from screen
38. Kinetic perimetry entails moving a test object
along various meridians and noting when it is
detected.
E.g., Goldmann
White and colored test objects varying in size
from 1 mm to 5 mm
Smaller test object, smaller VF.
If size of a VF defect is same with all test
objects-steep, or abrupt, margins.
If larger with smaller test objects-gradual, or
sloping margins
39. Automated static perimetry
Humphrey Visual Field Analyzer
Normal patients may appear to have
abnormal VF due to large number of
erroneous responses that can occur during
automated testing
40.
41.
42. Direct opthalmoscopy
Small aperture-examining an undilated pupil,
large aperture-dilated pupil
Red-free filter-examining blood vessels,
looking for hemorrhages, and nerve fiber
layer
Red reflex-assessed from distance of 12 in to
15 in.
Areas of primary concern- disc, macula, and
arteries
43. Disc normally round or vertically oriented
slight oval.
Nasal margin slightly blurred
Peripheral neuroretinal rim and central cup.
Physiologic cup-slight depression in center of
disc that is less pinkish than rim and shows a
faint latticework due to underlying lamina
cribrosa.
Rim is elevated slightly above cup.
44. Myelinated axons-normal optic disc yellowish
white.
Paler temporally where papillomacular bundle
(PMB) enters.
When scleral opening small, disc consists
entirely of neuroretinal tissue, and
inconspicuous or nonexistent cup.
More vulnerable to anterior ischemic optic
neuropathy-disc at risk.
Normal cup-to-disc ratio-0.1 to 0.5.
45. Macula-dark area that lies about 2 disc
diameters temporal to and slightly below
disc.
Appears darker than surrounding retina
because of thinner retina
Area of macula devoid of large blood vessels.
Fovea centralis appears pinpoint of light
reflected from center of macula.
Macula may be seen more easily with a red-
free filter, if patient looks directly into light
46. Photostress Test
In macular disease, photoreceptors require
longer to recover from bleaching of retinal
pigments after exposure to a bright light.
Baseline visual acuity
Then shining a bright light (e.g., a fresh penlight)
into eye for 10 seconds
Determine time required for visual acuity to
return to baseline.
Mainly useful with unilateral disease
Optic nerve disease-normal photostress test.
47. Papilledema Four stages of -early, fully
developed, chronic, and atrophic.
Fully developed-elevation of disc surface,
humping of vessels crossing disc margin,
obliteration of disc margins, peripapillary
hemorrhages, cotton wool exudates,
engorged and tortuous retinal veins, and
marked disc hyperemia
Early papilledema-loss of previously observed
spontaneous venous pulsations (SVPs).
SVPs=200 mm H2O ICT
48. Pseudopapillodema
Common causes-optic nerve drusen,
myelinated nerve fibers, remnants of
primitive hyaloid artery (Bergmeister's
papilla), tilted discs, extreme hyperopia.
Optic nerve drusen, or hyaloid bodies
◦ Acellular, calcified hyaline deposits within optic
nerve that may elevate and distort disc.
◦ Present 2%, bilateral in 70%
◦ Highly refractile, rock-candy appearance.
49. In papilledema-
1. disc is usually hyperemic;
2. margin blurriness at superior and inferior poles early
in process;
3. blood vessels look normal except for fullness of veins;
4. NFL is dull with retinal blood vessels obscured because
of retinal edema.
In pseudopapilledema
1. disc color remains normal;
2. blurriness of disc margin may be irregular,disc may
have a lumpy appearance;
3. blood vessels on the disc frequently look anomalous;
4. NFL is clear.
If in doubt, consult an ophthalmologist.
57. Inderbir Singh's Textbook of Human
Neuroanatomy (Fundamental and Clinical)
DeJong’s The Neurological Examination, Sixth
Edition
Optic Nerve: Anatomy, Function, And
Common Disorders;edward A. Margolin,
Rajeshvar K . Sharda;Ophthlmology Rounds;
May/June 2014 Volume 6, Issue 3
The optic nerve: a clinical
perspective;Pasquale Montaleone;UWOMJ |
79:2 | Fall 2012
Editor's Notes
A. Central scotoma B. Cecocentral scotoma C. Junctional scotoma D. Homonymous scotomas
E. Heteronymous scotomas F. Right homonymous hemianopia G. Bitemporal hemianopia H. Congruous right homonymous hemianopia I.
Incongruous right homonymous hemianopia J. Right superior quadrantopia (“pie in the sky”) K. Right inferior quadrantopia L.
Macular-sparing right homonymous hemianopia.