DrVinit Suri is one of the most eminent neurologists in India with more than 30 years of experience in the field. He is a graduate of University College of Medical Sciences, Delhi University and stood first in the Final MBBS examination with several gold medals to his credit and obtained his D.M. Neurology from G.B.Pant Hospital in 1992.He has been involved in teaching graduate and postgraduate students since last 30 years and this is something very close to his heart . He is extremely sought after by his students for teaching neurological examination methods and skills of localization in simple and easy to understand manner.
This book will provide a concise, focused overview of methods of neurological examination, enabling a focused clinical approach for localization in patients with neurological disorders. Chapters provide a systematic approach for clinical examination along with essential aspects of the neuro-anatomy to provide specific information about disease localization. This book assists medical students pursuing DM/DNB- Neurology, MCH -Neurosurgery, MD/DNB- Internal medicine, MBBS students, and Clinicians, including Neurologists, Neurosurgeons, Internal medicine physicians, and other neuro-scientists. It provides a unique opportunity to formulate correct concepts for clinical neurological examination and hence localization but also provides the opportunity to quickly revise the entire book in a short time.
Vinit Suri is one of the most eminent neurologists in India with more than 34 years of experience in the field. He has been actively involved in teaching graduate and postgraduate students since the last 30 years and this is something very close to his heart. He has been working at Indraprastha Apollo Hospital, New Delhi, as Senior Consultant Neurologist and Coordinator of the department since 1996 and is the Academic Advisor running the Neurology DNB teaching Program. He has been conferred the title of Distinguished Clinical Tutor and Professor of Medicine by the AHERF Apollo Hospitals Educational & Research Foundation.He has served the Indian Stroke Association as the Secretary, Treasurer, and President and the Delhi Neurological Association as its President.
The neurological examination is an assessment tool to determine a patient's neurologic function. It is beneficial in a variety of ways as it allows the localization of neurologic diseases and helps in ruling in or ruling out differential diagnoses. Neurological diseases can present a myriad of ways, including cognitive/behavioral, visual, motor, and sensory symptoms. Certain red flags during examination allow early detection of life-threatening neurologic diseases and recognize disorders that may negatively impact the quality of life.[1]
The neurologic examination is useful in both ambulatory and emergency settings. It provides the physician a tool to recognize neurologic involvement in certain disease states, and thereby allow proper work-up and treatment for these patients. It is also beneficial in intensive care units, particularly in monitoring neurologic sequelae of diseases like strokes, intracranial tumors, and traumatic brain injury.[2][3] In emergent settings, rapid assessment of the severity of an injury and neurologic involvement is crucial and leads to fast decision-making in patient management, as well as improvement of patient survival rates.[4]
The neurological exam can be intimidating and challenging to perform for most physicians. It is particularly challenging to perform in certain age groups like infants, younger children, and older uncooperative adults.[5] In the examination of a pediatric patient, proper diagnoses begin with understanding which specific age groups are prone to developing certain disease processes. It is also important to keep in mind that the manifestation of certain neurologic illnesses can be vastly different in children and adults.
Physicians encounter an extensive range of patients with different illnesses daily. These can range from relatively benign to life-threatening conditions. This range of potentials highlights the importance of a physician's ability to recognize red flags early on in the disease processes. These red flags are picked up in history or during a neurological examination. A good example would be a patient who presents with chronic headaches, which can be a benign condition like migraine or life-threatening like a tumor. The presence of nausea and vomiting in the patient's history may still be present in migraines or may be a sign of increased intracranial pressure. An abnormal neurological examination can then direct the physician to the diagnosis (e.g., ataxic gait in this patient points to a cerebellar lesion). The physician can then refer the patient for appropriate diagnostic imaging and direct the management.[7]
Recognizing red flags can be challenging for physicians, particularly when it comes to neurologically related disorders. The complexity of the neurologic examination, the interpretation of results, and the correlation to the neuroaxis are often challenging. This fact highlights the need for increased awareness of what constitutes a proper neurological examination and what each specific finding suggests. It is also important to note that some positive results, especially in isolation, can be a normal variant.
A neurological examination should also be tailored and focused on specific disease presentations. Certain maneuvers can be incorporated to increase the sensitivity of an exam for a certain symptom; an elderly patient with memory deficits will require a more in-depth cognitive assessment than a young patient with ptosis.
A basic neurologic examination can be performed rapidly with practice. The presence of an abnormal result usually warrants further investigation and referrals to specific specialties. It helps to recognize and therefore manage diseases earlier in their course. A complete neurologic examination should contain an assessment of sensorium, cognition, cranial nerves, motor, sensory, cerebellar, gait, reflexes, meningeal irritation, and long tract signs. Specific scales are useful to improve interobserver variability.
The cranial nerves innervate the structures in the head and neck. The olfactory nerve and optic nerve exit from the cerebrum. The cranial nerves 3 to 12 exit from the brainstem. Abnormality in cranial nerve function helps in localizing the lesion to a specific level of the brain or brainstem. Cranial nerves have motor, sensory and autonomic functions. It is important to note that, in general, a singular cranial nerve deficit points to a lesion of the peripheral nerve. A lesion in the brainstem, being a busy structure, will involve multiple cranial nerve deficits, as well as motor and sensory tracts to the extremities.
Olfactory nerve (Cranial nerve I) - This is the least tested of cranial nerves in the clinical setting. To test function involves the assessment of the patient's sense of smell. Start with one nostril while covering the opposing nostril to allow for proper detection of any abnormal findings. Do this for both sides. The most common causes of anosmia, the loss of smell, are the following: infections, allergies, or nasal polyps. Other causes include trauma (fracture of the cribriform plate), Parkinson disease, lesions at the base of the skull (meningioma), or rare genetic conditions.[10]
Oculomotor, trochlear, and abducens nerves (Cranial nerve III, IV, and VI) are the nerves for extraocular muscle movement. Assessment involves drawing an invisible "H" in front of the patient and asking the patient to follow with their eyes. Abnormal findings present as disconjugate gaze or double vision. The involvement of the third cranial nerve by compression (aneurysm of the posterior communicating artery) leads to dilated pupil, ptosis, and eyes looking outward and downward. Lateral rectus palsy is due to the involvement of the sixth cranial nerve; it can be a false localizing sign in increased intracranial pressure (bilateral lateral rectus palsy). The involvement of the pathways in the brainstem (e.g., lacunar infarct, multiple sclerosis) can lead to internuclear ophthalmoplegia. This condition occurs when the medial longitudinal fasciculus (MLF), a heavily myelinated pathway that allows for coordinated horizontal gaze, is damaged.[13]
The facial nerve (Cranial nerve VII) supplies the muscles of facial expression, stapedius muscle, and taste to the anterior two- of the tongue. Assessment of this nerve involves asking the patient to move their facial muscles by asking them to raise their eyebrows, close their eyes tightly, smile, and blow up their cheeks. The location of weakness in facial muscles can differentiate between peripheral or central involvement. A weakness with the movement of the entire right side of the face is indicative of either a peripheral lesion or damage to the facial nucleus on the ipsilateral side, like in Bell's palsy or a pontine infarct. A weakness of the lower half of the face with sparing of the forehead is suggestive of a lesion above and contralateral to the facial nerve (stroke involving the motor cortex). This is because the forehead has innervation from both the left and right sides of the motor cortex. [15] Damage to the facial nerve can also present with hyperacusis and loss of taste to the anterior 2/3 of the tongue.
The vestibulocochlear nerve (Cranial nerve VIII) supplies functions in hearing and equilibrium. Gross assessment of function can be done by whispering words behind the patient, rubbing fingers or hair together close to the ear, and asking if the patient can hear. If a hearing deficit is established, doing a Weber and Rinne test can differentiate sensorineural from conductive hearing loss. A normal Rinne exam will exhibit air conduction (AC) greater than bone conduction (BC). A conductive hearing loss will show BC greater than AC. In patients with sensorineural hearing loss, AC will be greater than BC, but for a shorter duration when compared to a normal subject. A normal Weber test shows hearing the sound/vibration equally in both ears. A conductive hearing loss will lateralize the sound to the abnormal ear while a sensorineural hearing loss will lateralize to the normal ear.[16]
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