NervousSystem

Anatomy and pathology of the nervous system is understood by directly visualizing it. This is best accomplished by handling the brain (or model of the brain as the case may be) and dissecting or taking it apart for direct examination. The purpose (for the clinician) of understanding neuroanatomy and neurophysiology is to be able to use that knowledge to solve clinical problems. The first step in solving a clinical problem is anatomical localization. So, if one cannot directly inspect the patient's brain, how is this localization accomplished? The "window" to the patient's brain is the neurological examination. The neuro exam is a series of tests and observations that reflects the function of various parts of the brain. If the exam is approached in a systematic and logical fashion that is organized in terms of anatomical levels and systems then the clinician is lead to the anatomical location of the patient's problem.  

Introduction Examination of the cranial nerves allows one to "view" the brainstem all the way from its rostral to caudal extent. The brainstem can be divided into three levels, the midbrain, the pons and the medulla. The cranial nerves for each of these are: 2 for the midbrain (CN 3 & 4), 4 for the pons (CN 5-8), and 4 for the medulla (CN 9-12). It is important to remember that cranial nerves never cross (except for one exception, the 4th CN) and clinical findings are always on the same side as the cranial nerve involved. Cranial nerve findings when combined with long tract findings (corticospinal and somatosensory) are powerful for localizing lesions in the brainstem. Cranial Nerve 1 Olfaction is the only sensory modality with direct access to cerebral cortex without going through the thalamus. The olfactory tracts project mainly to the uncus of the temporal lobes. Cranial Nerve 2 This cranial nerve has important localizing value because of its "x" axis course from the eye to the occipital cortex. The pattern of a visual field deficit indicates whether an anatomical lesion is pre- or postchiasmal, optic tract, optic radiation or calcarine cortex. Cranial Nerve 3 and 4 These cranial nerves give us a view of the midbrain. The 3rd nerve in particular can give important anatomical localization because it exits the midbrain just medial to the cerebral peduncle. The 3rd nerve controls eye adduction (medial rectus), elevation (superior rectus), depression (inferior rectus), elevation of the eyelid (levator palpebrae superioris), and parasympathetics for the pupil. The 4th CN supplies the superior oblique muscle, which is important to looking down and in (towards the midline). Pontine Level Cranial nerves 5, 6, 7, and 8 are located in the pons and give us a view of this level of the brainstem. Cranial Nerve 6 This cranial nerve innervates the lateral rectus for eye abduction. Remember that cranial nerves 3, 4 and 6 must work in concert for conjugate eye movements; if they don't then diplopia (double vision) results. The medial longitudinal fasciculus (MLF) connects the 6th nerve nucleus to the 3rd nerve nucleus for conjugate movement. Major Oculomotor Gaze Systems Eye movements are controlled by 4 major oculomotor gaze systems, which are tested for on the neurological exam. They are briefly outlined here: Saccadic (frontal gaze center to PPRF (paramedian pontine reticular formation) for rapid eye movements to bring new objects being viewed on to the fovea. Smooth Pursuit (parietal-occipital gaze center via cerebellar and vestibular pathways) for eye movements to keep a moving image centered on the fovea. Vestibulo-ocular (vestibular input) keeps image steady on fovea during head movements. Vergence (optic pathways to oculomotor nuclei) to keep image on fovea predominantly when the viewed object is moved near (near triad- convergence, accommodation and pupillary constriction) Cranial Nerve 5 The entry zone for this cranial nerve is at the mid pons with the motor and main sensory (discriminatory touch) nucleus located at the same level. The axons for the descending tract of the 5th nerve (pain and temperature) descend to the level of the upper cervical spinal cord before they synapse with neurons of the nucleus of the descending tract of the 5th nerve. Second order neurons then cross over and ascend to the VPM of the thalamus. Cranial Nerve 7 This cranial nerve has a motor component for muscles of facial expression (and, don't forget, the strapedius muscle which is important for the acoustic reflex), parasympathetics for tear and salivary glands, and sensory for taste (anterior two-thirds of the tongue). Central (upper motor neuron-UMN) versus Peripheral (lower motor neuron-LMN) 7th nerve weakness- with a peripheral 7th nerve lesion all of the muscles ipsilateral to the affected nerve will be weak whereas with a "central 7th ", only the muscles of the lower half of the face contralateral to the lesion will be weak because the portion of the 7th nerve nucleus that supplies the upper face receives bilateral corticobulbar (UMN) input. Cranial Nerve 8 This nerve is a sensory nerve with two divisions- acoustic and vestibular. The acoustic division is tested by checking auditory acuity and with the Rinne and Weber tests. The vestibular division of this nerve is important for balance. Clinically it be tested with the oculocephalic reflex (Doll's eye maneuver) and oculovestibular reflex (ice water calorics). Medullary Level Cranial nerves 9,10,11, and 12 are located in the medulla and have localizing value for lesions in this most caudal part of the brainstem. Cranial nerves 9 and 10 These two nerves are clinically lumped together. Motor wise, they innervate pharyngeal and laryngeal muscles. Their sensory component is sensation for the pharynx and taste for the posterior one-third of the tongue. Cranial Nerve 11 This nerve is a motor nerve for the sternocleidomastoid and trapezius muscles. The UMN control for the sternocleidomastoid (SCM) is an exception to the rule of the ipsilateral cerebral hemisphere controls the movement of the contralateral side of the body. Because of the crossing then recrossing of the corticobulbar tracts at the high cervical level, the ipsilateral cerebral hemisphere controls the ipsilateral SCM muscle. This makes sense as far as coordinating head movement with body movement if you think about it (remember that the SCM turns the head to the opposite side). So if I want to work with the left side of my body I would want to turn my head to the left so the right SCM would be activated. Cranial Nerve 12 The last of the cranial nerves, CN 12 supplies motor innervation for the tongue. Traps A 6th nerve palsy may be a "false localizing sign". The reason for this is that it has the longest intracranial route of the cranial nerves, therefore it is the most susceptible to pressure that can occur with any cause of increased intracranial pressure.  

Cranial Nerve 1- Olfaction This patient has difficulty identifying the smells presented. Loss of smell is anosmia. The most common cause is a cold (as in this patient) or nasal allergies. Other causes include trauma or a meningioma affecting the olfactory tracts. Anosmia is also seen in Kallman syndrome because of agenesis of the olfactory bulbs. Cranial Nerve 2- Visual acuity This patientâs visual acuity is being tested with a Rosenbaum chart. First the left eye is tested, then the right eye. He is tested with his glasses on so this represents corrected visual acuity. He has 20/70 vision in the left eye and 20/40 in the right. His decreased visual acuity is from optic nerve damage. Cranial Nerve II- Visual field The patient's visual fields are being tested with gross confrontation. A right sided visual field deficit for both eyes is shown. This is a right hemianopia from a lesion behind the optic chiasm involving the left optic tract, radiation or striate cortex. Cranial Nerve II- Fundoscopy The first photograph is of a fundus showing papilledema. The findings of papilledema include 1. Loss of venous pulsation 2. Swelling of the optic nerve head so there is loss of the disc margin 3. Venous engorgement 4. Disc hyperemi 5. Loss of the physiologic cup an 6. Flame shaped hemorrhages. This photograph shows all the signs except the hemorrhages and loss of venous pulsations. The second photograph shows optic atrophy, which is pallor of the optic disc resulting form damage to the optic nerve from pressure, ischemia, or demyelination. Images Courtesy Dr. Kathleen Digre, University of Uta Cranial Nerves 2 & 3- Pupillary Light Refle The swinging flashlight test is used to show a relative afferent pupillary defect or a Marcus Gunn pupil of the left eye. The left eye has perceived less light stimulus (a defect in the sensory or afferent pathway) then the opposite eye so the pupil dilates with the same light stimulus that caused constriction when the normal eye was stimulated. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Inspection & Ocular Alignmen This patient with ocular myasthenia gravis has bilateral ptosis, left greater than right. There is also ocular misalignment because of weakness of the eye muscles especially of the left eye. Note the reflection of the light source doesn't fall on the same location of each eyeball. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Versions • The first patient shown has incomplete abduction of her left eye from a 6th nerve palsy. • The second patient has a left 3rd nerve palsy resulting in ptosis, dilated pupil, limited adduction, elevation, and depression of the left eye. Second Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Duction Each eye is examined with the other covered (this is called ductions). The patient is unable to adduct either the left or the right eye. If you watch closely you can see nystagmus upon abduction of each eye. When both eyes are tested together (testing versions) you can see the bilateral adduction defect with nystagmus of the abducting eye. This is bilateral internuclear ophthalmoplegia often caused by a demyelinating lesion effecting the MLF bilaterally. The adduction defect occurs because there is disruption of the MLF (internuclear) connections between the abducens nucleus and the lower motor neurons in the oculomotor nucleus that innervate the medial rectus muscle. Saccades Smooth Pursui The patient shown has progressive supranuclear palsy. As part of this disease there is disruption of fixation by square wave jerks and impairment of smooth pursuit movements. Saccadic eye movements are also impaired. Although not shown in this video, vertical saccadic eye movements are usually the initial deficit in this disorder. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Utah Optokinetic Nystagmu This patient has poor optokinetic nystagmus when the tape is moved to the right or left. The patient lacks the input from the parietal-occipital gaze centers to initiate smooth pursuit movements therefore her visual tracking of the objects on the tape is inconsistent and erratic. Patients who have a lesion of the parietal-occipital gaze center will have absent optokinetic nystagmus when the tape is moved toward the side of the lesion. Vestibulo-ocular refle The vestibulo-ocular reflex should be present in a comatose patient with intact brainstem function. This is called intact "Doll’s eyes" because in the old fashion dolls the eyes were weighted with lead so when the head was turned one way the eyes turned in the opposite direction. Absent "Doll’s eyes" or vestibulo-ocular reflex indicates brainstem dysfunction at the midbrain-pontine level. Vergenc Light-near dissociation occurs when the pupils don't react to light but constrict with convergence as part of the near reflex. This is what happens in the Argyll-Robertson pupil (usually seen with neurosyphilis) where there is a pretectal lesion affecting the retinomesencephalic afferents controlling the light reflex but sparing the occipitomesencephalic pathways for the near reflex. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerve 5- Sensor There is a sensory deficit for both light touch and pain on the left side of the face for all divisions of the 5th nerve. Note that the deficit is first recognized just to the left of the midline and not exactly at the midline. Patients with psychogenic sensory loss often identify the sensory change as beginning right at the midline. Cranial Nerves 5 & 7 - Corneal refle A patient with an absent corneal reflex either has a CN 5 sensory deficit or a CN 7 motor deficit. The corneal reflex is particularly helpful in assessing brainstem function in the unconscious patient. An absent corneal reflex in this setting would indicate brainstem dysfunction. Cranial Nerve 5- Motor • The first patient shown has weakness of the pterygoids and the jaw deviates towards the side of the weakness. • The second patient shown has a positive jaw jerk which indicates an upper motor lesion affecting the 5th cranial nerve. First Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 7- Motor • The first patient has weakness of all the muscles of facial expression on the right side of the face indicating a lesion of the facial nucleus or the peripheral 7th nerve. • The second patient has weakness of the lower half of his left face including the orbicularis oculi muscle but sparing the forehead. This is consistent with a central 7th or upper motor neuron lesion. Video Courtesy of Alejandro Stern, Stern Foundatio Cranial Nerve 7- Sensory, Tast The patient has difficulty correctly identifying taste on the right side of the tongue indicating a lesion of the sensory limb of the 7th nerve. Cranial Nerve 8- Auditory Acuity, Weber & Rinne Test This patient has decreased hearing acuity of the right ear. The Weber test lateralizes to the right ear and bone conduction is greater than air conduction on the right. He has a conductive hearing loss. Cranial Nerve 8- Vestibula Patients with vestibular disease typically complain of vertigo – the illusion of a spinning movement. Nystagmus is the principle finding in vestibular disease. It is horizontal and torsional with the slow phase of the nystagmus toward the abnormal side in peripheral vestibular nerve disease. Visual fixation can suppress the nystagmus. In central causes of vertigo (located in the brainstem) the nystagmus can be horizontal, upbeat, downbeat, or torsional and is not suppressed by visual fixation. Cranial Nerve 9 & 10- Moto When the patient says "ah" there is excessive nasal air escape. The palate elevates more on the left side and the uvula deviates toward the left side because the right side is weak. This patient has a deficit of the right 9th & 10th cranial nerves. Video Courtesy of Alejandro Stern, Stern Foundatio Cranial Nerve 9 & 10- Sensory and Motor: Gag Refle Using a tongue blade, the left side of the patient's palate is touched which results in a gag reflex with the left side of the palate elevating more then the right and the uvula deviating to the left consistent with a right CN 9 & 10 deficit. Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 11- Moto When the patient contracts the muscles of the neck the left sternocleidomastoid muscle is easily seen but the right is absent. Looking at the back of the patient, the left trapezius muscle is outlined and present but the right is atrophic and hard to identify. These findings indicate a lesion of the right 11th cranial nerve. Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 12- Moto Notice the atrophy and fasciculation of the right side of this patient's tongue. The tongue deviates to the right as well because of weakness of the right intrinsic tongue muscles. These findings are present because of a lesion of the right 12th cranial nerve.  

Connecting routes in the central nervous system. This include some neuro anatomy on the brain stem, cranial nerves and peripheral nervous system  

The process of neurulation drives development of the system we use to help understand and interact with the world around us. Sometimes this process might stray from its chosen path due to internal/external factors, leading to unusual pathologies. Understanding neurulation can help us work out how things go wrong.  

In Part 1 of Professor Fink's 2-Part Series on the Spinal Cord, he reviews the anatomy of the Spinal Cord and the functional organization at each segmental level. Professor Fink describes the horizontal flow of sensory information into the Spinal Cord and the flow of motor commands out of the Spinal Cord. Reference is made to Gray Matter, White Matter, Spinal Nerves, Dorsal Root Ganglion, Ventral Root, Commissures, decussation, Somatic Reflexes, Dorsal (Posterior) Gray Horn, Ventral (Anterior) Gray Horn, Lateral Gray Horn. Check-out professor fink's web-site or additional resources in Biology, Anatomy, Physiology & Pharmacology: www.professorfink.com Lecture Outlines by Professor Fink can be purchased from the WLAC Bookstore at: http://onlinestore.wlac.edu/fink.asp  

http://www.handwrittentutorials.com - This tutorial looks at the ways in which the Nervous System is divided and categorised, both functionally and anatomically. Concepts such as the CNS, PNS and the Autonomic Nervous system are discussed in detail. For more entirely FREE tutorials and the accompanying PDFs visit http://www.handwrittentutorials.com  

Explains how the resting membrane potential is maintained. And how the ion concentration is, as it is at rest. http://www.facebook.com/ArmandoHasudungan PDF: https://docs.google.com/open?id=0B8Ss3-wJfHrpcG9SaDRwSHdpVUk  

Introduces the nervous system briefly, and mainly talk about the defenses of the nervous system as well as the glia cells which play roles in it.  

Nervous System, Neural Tissue, Neurons, Neuroglia, Conduction, Depolarization, Repolarization, Transmembrane Potential, Saltatory Propagation, Continuous Propagation  

 

Anatomy and Physiology, help, spinal cord, neural tissue, pia mater, dermatomes, dura mater, arachnoid mater, spinal anatomy, cauda equina, filum terminale, ganglia, dorsal root, ventral root, nervous system.  

Learn about the blood supply to the spinal cord in this 3D video anatomy tutorial.  

There are two types of neurofibromatosis, both inherited in an autosomal dominant manner, although some cases arise from spontaneous mutation. It results in benign tumours of the nervous system and bony and dermatological deformities.   Type I Neurofibromatosis – NF1 – aka von Recklinghausen’s disease  

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