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.
almost 9 years ago
The reference given when answering the question about the increase in permeability of sodium ions during hypocalcemia is satisfactory but "does hypocalcemia not reduce the release of neurotransmitters at a chemical synapse" Will it not affect the speed and efficiency of conduction of impulse. Therefore how will it cause tetany?" Reference Increased Permeability of the Sodium Channels When There Is a Deficit of Calcium Ions. The concentration of calcium ions in the extracellular fluid also has a profound effect on the voltage level at which the sodium channels become activated. When there is a deficit of calcium ions, the sodium channels become activated (opened) by very little increase of the membrane potential from its normal, very negative level. Therefore, the nerve fiber becomes highly excitable, sometimes discharging repetitively without provocation rather than remaining in the resting state. In fact, the calcium ion concentration needs to fall only 50 per cent below normal before spontaneous discharge occurs in some peripheral nerves, often causing muscle “tetany.”This is sometimes lethal because of tetanic contraction of the respiratory muscles. The probable way in which calcium ions affect the sodium channels is as follows:These ions appear to bind to the exterior surfaces of the sodium channel protein molecule. The positive charges of these calcium ions in turn alter the electrical state of the channel protein itself, in this way altering the voltage level required to open the sodium gate. From: Guyton, Arthur C. Textbook of medical physiology / Arthur C. Guyton, John E. Hall.—11th ed.
almost 7 years ago
http://www.anatomyzone.com Anatomy tutorial on the basic structure of the synapse. This video doesn't cover action potential generation or detailed mechanism...
almost 5 years ago
SMACC Chicago 2015 : A Different (and very personal) Perspective Crystal Upshaw RN EHS LIFEFLIGHT Nova Scotia Canada I have read many excellent summaries of the SMACC Chicago experience. They included wonderful synapses and learning points from the conference. I have nothing to add in that regard-all the best points have been covered. Ever since…
over 4 years ago
In 1907, the British physiologist John N. Langley introduced the concept of receptor molecules to explain the specific and potent actions of certain chemicals on muscle and nerve cells. Much subsequent work has shown that receptor molecules do indeed account for the ability of neurotransmitters, hormones, and drugs to alter the functional properties of neurons. While it has been clear since Langley's day that receptors are important for synaptic transmission, their identity and detailed mechanism of action remained a mystery until quite recently. It is now known that neurotransmitter receptors are proteins embedded in the plasma membrane of postsynaptic cells. Domains of receptor molecules that extend into the synaptic cleft bind neurotransmitters that are released into this space by the presynaptic neuron. The binding of neurotransmitters, either directly or indirectly, causes ion channels in the postsynaptic membrane to open or close (Figure 7.1). Typically, the resulting ion fluxes change the membrane potential of the postsynaptic cell, thus mediating the transfer of information across the synapse. Figure 7.1Receptors that mediate the postsynaptic actions of neurotransmitters have two functions. First, specific binding sites on the extracellular side of receptors allow these proteins to detect the presence of neurotransmitters in the synaptic cleft. Second, transmitter-bound receptors alter the ionic permeability of the postsynaptic membrane by virtue of being coupled, directly or indirectly, to ion channels in the postsynaptic membrane. Opening or closing these channels as a result of transmitter binding allows ionic currents to flow, thus changing the postsynaptic membrane potential.
over 4 years ago
Visual Processing: Cortical Pathways (Section 2, Chapter 15) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston
The visual system is unique as much of visual processing occurs outside the brain within the retina of the eye. The previous chapter described how the light-sensitive receptors of the eye convert the image projected onto the retina into spatially distributed neural activity in the first neurons of the visual pathway (i.e., the photoreceptors). Within the retina, the receptors synapse with bipolar and horizontal cells, which establish the basis for brightness and color contrasts. In turn, the bipolar cells (the 2° visual afferent) synapse with retinal ganglion cells and amacrine cells, which enhance contrast effects that support form vision and establish the basis for movement detection. The information from the eye is carried by the axons of the retinal ganglion cells (the 3° visual afferent) to the midbrain and diencephalon. This chapter will provide more information about visual pathway organization and the visual processing that occurs within the brain.
over 4 years ago