Pediatrics: Cranial Nerve Examination Essay

INTRODUCTION. Idiopathic congenital nystagmus, or idiopathic infantile nystagmus is a disease characterized by the rapid, involuntary eye movement. This movement is typically in the horizontal direction, however, movement in other directions have been observed. One way to get nystagmus is through genetic mutations. Nystagmus caused by genetic mutation is seen at a relatively young age but cannot yet be treated. The disease is not understood well, it is believed that the cause is a developmental defect. The linkage, and inheritance has not been identified, the patterns suggest that multiple genes are involved in the disease and that there are loci on different chromosomes with three of the five loci located on the X chromosome. Mutations have been linked to the FRMD7 gene, a gene that consists of 12 exons, of the FERM family. The function of FRMD7 have yet to be determined however an abundance of the protein in the brain in areas associated with the eye. Mutations within this region consist of missense, deletion, tranversion and nonsense mutations. Over forty-four mutations that lead to ICN have been found in the FRMD7 gene. Learning more about the mutation of FRMD7 in ICN is important because these mutations may prevent elongation of neurite processes during differentiation preventing axons from responding to stimuli (Watkins et al. 2012).

The human body is made up of many organ systems that consist of organs and tissues of different anatomies and diverse nomenclature. These organs systems, organs and tissues are prone to thousands of diseases, and one of these diseases is cerebral palsy, which is a disease of the nervous system in simple terms. Research relating to cerebral palsy is carried out, whereby the disorder is described, along with its history, and how it affects the nervous system and the brain. The anatomy of the body systems involves with regard to this disorder, the effects of the disorder on these body systems and other body systems are also researched and discussed. Furthermore, the research focuses on the causes of cerebral palsy, its complications, signs, and symptoms, and the diagnosis of the disorder, along with its treatment and side effects of the treatment. A recap of the research focusing on prevention strategies, the anatomy and physiology of cerebral palsy and the nervous system is presented.

Visual fields full to confrontation. Extraocular muscles intact. PERRLADC. Normal facial symmetry, sensation and movement. Tongue and uvula were midline. Normal auditory acuity. Shoulder shrug is normal.

PPO Jimenez put Garduno in the “starting position”. PPO Jimenez held a pen in a position in front of Garduno’s face and asked him to track the pen with his eyes only. Garduno acknowledged that he understood the instructions. During the Horizontal Gaze Nystagmus test PPO Jimenez noticed Garduno had a lack of smooth pursuit in both eyes. PPO Jimenez also noticed that Garduno had a distinct and sustained Nystagmus as maximum deviation in both eyes. Additionally PPO Jimenez noticed Garduno had the onset of nystagmus prior to 45-degree angle in both eyes. After PPO Jimenez observed Garduno fail this test he decided not to continue with the walk and turn test and one leg stand due to the physical condition of Garduno.

-The doctor will go through the same steps, but with the left eye is covered now. -Results will be recorded. The Oculomotor Nerve III is tested.

It also allows for the front part of the tongue to sense taste and the eyes to open and close. This nerve is located in the Fallopian canal of the skull, inferior to the ear and bilaterally connected to the muscles of the face. (PEDIACTRICS Vol. 112 No. 2, 2003). It is thought that with the incidence of Lyme disease, the inflammation correlated with the disease is the cause of Bell’s palsy because of the pressure it puts on this nerve.

Visual fields full to confrontation. Extraocular muscles intact. PERRLADC. Normal facial symmetry, sensation, and movement. Tongue and uvula were midline. Decreased auditory acuity bilaterally. Normal shoulder shrug.

                 Rett syndrome, including the age of onset and the severity of symptoms, varies from child to child. Before the symptoms begin, however, the child generally appears to grow and develop normally, although there are often subtle abnormalities even in early infancy, such as loss of muscle tone (hypotonia), difficulty feeding, and jerkiness in limb movements. Then, gradually, mental and physical symptoms appear. As the syndrome progresses, the child loses purposeful use of her hands and the ability to speak (Rett Syndrome, 2010). Other early symptoms may include problems crawling or walking and diminished eye contact (Rett Syndrome, 2010). The onset of a period of regression is sometimes sudden.  Apraxia — the inability to perform motor functions — is perhaps the most severely disabling feature of Rett syndrome, interfering with every body movement, including eye gaze

My interest in the anatomy of the eye began when I was a small child. I was 8 years old when my father experienced retinal detachment in the first eye. I didn’t understand a whole lot of what was happening when my brother and I were whisked up and on a plane to a hospital in Portland for surgery. During the long wait, my mother began describing what was happening in my father’s eye. I remember sitting and

I noticed nystagmus in both eyes at maximum deviation. Mcclellan also had involuntary movement in both eyes prior to 45 degrees.

Professor Roger Hugh Stephen Carpenter is an English neurophysiologist and a Professor of Oculomotor Physiology at the University of Cambridge. He recognises that head movements, both rotational and translational, stimulate the vestibulo ocular reflex.

Cranial Nerve II (Occipital nerve) is also sensory and conveys visual input. Cranial Nerve III (Oculomotor), IV (Trochlear) and VI (Abducens) control eye movement. Nerves III ,IV and VI are motor types of nerves. The oculomotor nerve (III) moves the eye and raises the eyelids as well as adjusts the lens and pupils of the eye. The Trochlear nerve (IV) controls the movement of the eyeball. The Abducens nerve (VI) moves the eyeballs outward. Cranial Nerve V (Trigeminal) is mixed (a mix of motor and sensory) and is divided into 3 parts: ophthalmic, maxillary and mandibular. This nerve controls the muscles of the face associated with chewing. Cranial Nerve V also controls feelings of the skin including pain and temperature. Cranial Nerve VII (Facial) is also mixed and controls facial movements. The facial nerve also controls saliva and tear

If you notice your little one scrunching his eyes when reading or watching TV, it’s a sure sign he needs to get an eye exam.

The fifth cranial nerve out of 12 is known as the trigeminal nerve. Cranial nerves are located in the brain and each have a different function. The trigeminal nerve is located in between the oculomotor nerve and the facial nerve. The trigeminal nerve performs sensor functions that involve the teeth, tongue, nose, and eyes and is covered by a myelin sheath. A myelin sheath is the protective coating that is usually found around nerves. Trigeminal neuralgia also known as TN, is a painful disease that affects the trigeminal nerve. The disorder causes severe, sporadic, sudden burning or shock-like face pain that can last as short as a few seconds to as long as two minutes per episode of pain. Patients suffering from the disorder may sometimes

One cause of strabismus is the inadequate coordination of the six muscles which operate to move the eye. Other less common forms of strabismus result from defective refraction, damaged nerves which connect the photoreceptors to the brain, and damage to the nerves which control the eye muscles.(4) These multiple disorders all have the same effect, presenting conflicting, amblyopic, images to the brain.