Eelco F.M. Wijdicks, M.D.
Mayo Medical Center
Professor of Neurology
Medical Director
Neurologic - Neurosurgical Care Unit
Saint Marys Hospital 

Starting in medical school neurologic examination has remained intimidating for many physicians. The examination has been perfected over many decades thanks to our French and German founding fathers. It has led to eponyms (e.g. - Babinski sign, Hoffmann reflex) different techniques of detecting subtle signs of weakness (e.g. - hand rolling, foot tapping) and even a wide collection of reflex hammers that can be proudly displayed in the office. How is one to summarize a skill or tool that can be directly used in daily practice? As with many medical specialties, the history is dependent on specific knowledge of neurologic disorders. And it has become a cliché to think that neurologic examination is dull and time consuming involving meticulous assessment of reflex asymmetries, sensory deficits and mental function. Some may argue whether a MRI would not suffice. Diagnostic tests have grown tremendously over the last decade and may have left the impression that neurologists, despite their acumen, may be inferior to them. Nothing seems further from the truth.

The level of this chapter will be for the medical student but also recently qualified physician in their first years of specialty training. Using the basic tenets of a comprehensive history, examination of the major components of brain, spinal cord, and neuromuscular unit function, a tentative diagnosis should be possible in approximately half of the cases. The principle of neurologic examination is localization of the lesion followed by a differential diagnosis of the cause of the lesion. This is a sacrosanct principle and cannot be ignored despite rapid development in technology. This chapter, however, has to ignore failure of some patients to describe a particular symptom, information forthcoming after repeated history and recognition of malingering. This chapter should have a practical value for the vast majority of physicians seeing patients in the clinic.

Sometimes one is not off to a good start. Patients may present their medical history illustrating a plethora of physician encounters, interpretation of diagnostic tests in layman terms, and multiple diagnoses often contradicting each other. As expected, many of the requests for a neurologic examination pertains to the infinite symptoms of dizziness, weakness, fatigue, facial numbness, confusion, and longstanding headache. The physician task is using a series of leading questions to obtain the overriding presenting symptom, onset and time, and its progression. Neurologic diseases may have different evolution over time. The onset can be acute which may be defined in seconds to rapidly progressing in hours, fluctuating typically over weeks, a relenting rapidly progressing course and a fluctuating, remitting and relapsing course such that is seen in multiple sclerosis and myasthenia gravis. In any presenting symptom, associated symptoms are of the utmost importance and many of them may involve systemic features such as fever, nausea and vomiting, or weight loss. The neurologic history remains time consuming but with quick pointers, one should be able to categorize a reliable account of the presentation. Family history is important in many neurologic disorders. A long list of genetic disorders has been described with a predominant neurologic presentation but many more of the common neurologic disorders run in families. These include hereditary peripheral neuropathy, multiple sclerosis, but also epilepsy, migraine, and cerebrovascular disease particularly intracranial aneurysms. The technique of history taking should remain respectful but may include prodding questions, constant verification of the answers, repetitive summaries to the patient and verification with family members.

Some leading questions are

1. Where in the body did it start?
2. When was the last time you were without any symptoms?
3. Why did it occur and are triggers known?
4. What did you do to relief the symptom?
5. How did it progress, evolve, came to a halt or improve?
6. Who was helping you out when it happened and what was done?

There are many, but only a few are common.

The cardinal features of headache are quality, severity, localization, relieving and precipitating factors, associated phenomena such as nausea or scotoma, as well as recurrence over time. The distinction between an acute and chronic persistent headache is usually easily apparent. Acute headache is often severe in intensity but acute should be further defined as split second (such as in a ruptured aneurysm), rapidly progressing (such as in migraine), or jabbing and jolting (such as in cluster headache and trigeminal neuralgia). The severity of pain is difficult to judge but it is important to know whether the pain is throbbing, lancinating, electric, stabbing, radiating, involving the entire head or unilateral, or more circumscript spots such as in a psychogenic headache. Factors that may aggravate the pain should be identified such as posture, straining, sneezing, coughing, movement, prior alcohol and even consumption of ice cream. Headache that changes with position is important. Many headaches associated with an increased intracranial pressure do worse with lying down and are severe at awakening in the morning and headaches associated with CSF hypotension are worse with standing up and immediately relieved with lying down. Headaches relieved with knee-chest position may be due to third ventricle obstructive tumors. The severity of the headache is difficult to measure. For example, a severe neck strain from overzealous gardening may look like an acute subarachnoid hemorrhage. Associated symptoms are important. Nausea and vomiting with acute new onset headache is commonly due to a structural lesion. Migraine may have specific features that may further classify the type of migraine such as aura (flickering lights, geometric distortions and even visual hallucinations), photophobia and sonophobia, and inability to accept any kitchen smells. Ptosis, nasal stuffing, redness of the conjunctiva may suggest a cluster headache. Electric lancinating pain in the cheek, ear, or jaw mimicking a molar abscess may suggest a trigeminal neuralgia. Touching the face with make up, a cold breeze, chewing or toothbrushing may trigger a brief lancinating electric stab as if a finger is put in a socket. It is sometimes a spot diagnosis. A patient who requires a dark room likely has migraine or chronic tension headache. A tendency to move, rock back and forth, is characteristic of a patient in the middle of a cluster headache, and a patient with trigeminal neuralgia may assume a typical posture in which the palm of the hand is held close to the cheek supported by the other arm but without touching it. It is important to find factors that may precipitate or aggravate headache and factors that may provide relief. Certain drugs may cause immediate relief and can be used as a diagnostic test. This includes several liters of nasal oxygen for cluster headache, any of the tryptans for classic migraine, and NSAIDs for paroxysmal hemicrania. Nonetheless it is important to mention that a rapid response to over-the-counter pain medications and even narcotics do not exclude the possibility of a more severe disorder such as brain tumor.

Neurologists are sometimes disillusioned when their clinic day only involves patients with dizziness and vertigo. As an isolated symptom it is rarely due to a neurologic cause. Dizziness is often described by the patient as wooziness, giddiness or faintness. In elucidating these umbrella terms it is important to determine whether the dizziness is true vertigo, in which the patient experiences a true rotational effect, or whether it consists of a light-headedness or presyncopal sensation. It is important to inquire about vertigo with other signs of brain stem dysfunction such as diplopia, dysarthria, dysphagia, hypesthesia, and acute ataxia. On the other hand the presence of ringing in the ear, hearing loss and violent vomiting may suggest a peripheral (labyrinth) rather than a central (brainstem) cause. Vertigo with position change is commonly due to a peripheral cause as well. Intermittent "dizzy spells" are commonly hyperventilation. Failure to perform a hyperventilation test (have the patient breathe in and out for one to two minutes trying to produce patients own recognizable symptoms) in these patients must be considered a mistake. In these dizzy patients who do not have the classic tingling fingers and tight lips during the attack a series of expensive MRI and ENT tests have been performed but they are only waiting to be recognized by an astute physician. Similarly it should be noted that some patients describe dizziness to point out a gait disorder and we have seen patients with early Parkinson’s disease and instability undergo several ENT evaluations until the tendency to pro- or retropulse or cogwheel rigidity is detected.

Numbness is vague term used by patients and may indicate weakness, pain or itching. True tingling, in which the patient describes a constant pins and needles sensation should be differentiated from a tight band, tight shoe, walking on air or rough surface sensation which indicates an abnormality in the posterior columns. Typically numbness has been present for quite some time in extremities. Extremity numbness expanding in a clockwise fashion, although sounding functional, may indicate a cervical spinal cord lesion. Lack of temperature sense needs to be addressed. Often patients are unable to distinguish hot and cold while taking a shower. Failure to recognize objects in a purse or in a pocket may also indicate significant loss of proprioception and is commonly found in a cervical spine lesion such as cervical spondylosis or syringomyelia. Some of these patients may demonstrate spontaneous finger movements in an attempt to orient them in space (pseudoathetosis).

Typically memory decline is a gradual process over years, but an alleged acute worsening may sometimes prompt early evaluation. Sometimes it is a child from out of state that visits after a while, only to find out that personal hygiene has tumbled downhill. In some patients family members are surprised that the patient does not know the date, the name of the president or any recent encounter when specifically asked. Memory decline often involves consistent difficulty with finding words, names, way to one’s own house, inability to describe routes to the clinic, but also more subtle problems such as inability to maintain a coherent conversation or failure to complete complex dinners.

A history of nocturnal confusion with wandering through the house and opening of drawers without a purpose may be obtained in a patient with advanced Alzheimer’s disease or any of the other dementias. Transient focal signs including dysarthria, aphasia, or hemiparesis may point to a multivascular dementia. A recent head trauma, often a car accident in the months before memory decline may indicate a subdural hematoma, and as expected it is not volunteered by the patient. Complete loss of memory is known as transient global amnesia and essentially the patient has no recollection of this episode. During this period the patient is constantly asking for where he is, whom he is with, and what he has been doing to be in this place. Complete loss of memory with a defined period of time, (or example, memory loss of three months) is typically psychogenic. Loss of moral behavior and critical judgment may indicate an advanced stage of dementia but depending on the underlying personality. Loss of a patient’s own identity is a very late stage of dementia often emerging when patients become bed - bound. Its early presentation should indicate pseudodementia. It is important to inquire about depressive symptoms such as anhedonia, weight loss, and suicidal thoughts to exclude the possibility of a treatable depression but patients with Alzheimers, particularly high strung individuals, may become depressed when defects are becoming noticed.

Speech disorders can be grossly distinguished between a dysarthria in which there is a major disturbance of articulation and aphasia in which the patient’s speech is distorted and words or letters become substituted. A dysarthria is not only slurring of words but also output is hesitant, explosive, and staccato. A fluent aphasia can be so severe ("word salad") that no content is discernible. The patient also then has difficulty with repetition and naming. A nonfluent aphasia is present when the speech is fragmentary, telegram style, with many substitutions and neologisms. Failure to speak (muteness) is uncommon but may occur in extreme advanced forms of Parkinson’s disease and due to bifrontal cerebral infarcts. Muteness with retained ability to recognize objects by word recognition and complete retention of writing is rarely structural and commonly psychogenic.

Weakness may involve one or two extremities. Unilateral weakness has more significance than a generalized sensation of weakness. In many patients, weakness is progressive; fluctuating weakness should point to the possibility of myasthenia gravis, particularly when it occurs after fatiguing the muscle. Again the time frame of weakness is important. Rapid onset weakness within days may indicate a Guillain - Barré syndrome, inflammatory myopathy, or a vasculitis. Unexplained weakness without any sensory symptoms in one or two limbs should point to the possibility of ALS and often the patient is not aware of associated fasciculations or muscle atrophy and will only indicate weight loss.

Visual abnormalities may involve blindness in one or both eyes, double vision, or blurring of vision. Blurring of vision in itself may indicate an intrinsic ophthalmological cause or inability of the patient to express diplopia. Diplopia is binocular, meaning that covering one eye will lead to its disappearance. In addition, degree of diplopia increases as the gaze proceeds in the direction of the action of the paralyzed muscle. Monocular blindness can be due to transient ischemic attack in the retina. This disorder presents with the gradual onset (minutes) of a full gray or black field and sometimes with a small peephole indicating macular sparing. In other patients an altitudinal hemianopia is seen in which the defining line between visual loss and normal vision is horizontal. An hemianopia is often homonymous, typically the left eye deals with vision to the left and the right eye to the right and examination will often delineate the visual fields defect. It is important to additionally inquire about eye pain. Optic neuritis or painful ophthalmoplegia due to cavernous sinus syndrome or migraine may all present with blindness.

Similar as in other branches of medicine, the occupation of the patient needs to be noted. Several neurologic disorders can be caused by poisons and heavy metal exposure. Lead, arsenic, insecticides, nitric oxide may all cause peripheral neuropathy. Drug-induced neurologic disorders are rare but many prescription drugs may have neurotoxic side effects. (An important reference is Neurotoxic Side Effects of Prescription Drugs.)  A history of a recent infectious diseases, insect bite, tropic travel, and previous hospitalizations should be included as well as a survey of the marital history, alcohol and drug use (alcohol causes subdural hematomas and ectasy or cocaine causes intracranial hemorrhages) when assessing a patient’s personality. Family history should be scrutinized for possible hereditary neurologic disorders (e.g. - Charcot - Marie -Tooth polyneuropathy, Huntington disease).

Neurologic examination follows a standardized pattern. Experience may tailor the full examination and result in focusing more on the most pertinent signs and symptoms. In addition often certain abnormalities should be reexamined over and over again to assure the abnormality.

Level of consciousness is measured with the Glasgow Coma Scale. This simple scoring system does not indicate the cause of decreased level of consciousness or coma but only indicates the depth of coma using three simple components. The spontaneous verbal eye and motor response is assessed followed by response to voice and pain. The pain stimulus is standardized using compression of the supraorbital nerve, nailbed, or temporomandibular joint. These noxious stimuli can produce standardized responses and these are outlined in the table.

Paradoxically the most severe form of coma, persistent vegetative state, the patient has the eyes open and will appear to look about but is unable to track any visual object (awake but not aware). Apart from determining the depth of coma it is important to evaluate hourly fluctuations. Fluctuation in level of consciousness may be caused sedative drugs, sleep deprivation but also by a disorder called nonconvulsive status epilepticus in which fluctuating level of consciousness is associated with eye lid jerking, staring as well as fumbling with hands and picking at clothes and bed linen. Overt jerking of extremities is not seen despite continuous electrographic spike and wave activity.

Cognitive function is tested using a series of batteries. Cognitive decline, as alluded to earlier, starts insidiously. In the very old (more than 85) a dividing line between dementia or some decline in memory function remains often difficult to draw. Several memory scales have been developed which test not only memory but also orientation, general knowledge, calculation, abstract thinking and so forth. Table 2 shows the individual components that are evaluated with a comprehensive bedside mental status examination.

Failure to perform any of those tests, but usually a combination, may indicate a cognitive decline and would justify more extensive psychometric testing. Other investigations of higher cortical function are important. Apraxia is due to a disturbance of skilled movement or due to a disconnection of the speech area in the area of cortex that integrates motor tasks. Patients are unable to perform tasks such as a salute, form interlocking fingers, comb hair, stick out tongue, or pucker as if to kiss.

The examination of 12 cranial nerves is simple in its execution but complex in interpretation.

Smell and taste is often impaired due to other systemic illnesses including banalities such as the flu. It is uncommonly tested during a routine neurologic examination but smell cards have been devised. Standard odors include peppermint, cloves, musk, and floral powders, as well as coffee and lemon extracts. The distinction between odors has more importance than its precise recognition. Anosmia can be excluded if the patient appreciates at least one odored powder. The abnormalities of the olfactory nerve are typically caused by severe traumatic brain injury or a meningioma arising from the olfactory groove.

The optic nerve is examined using several tests starting with visual acuity. Each eye is tested separately using Snellen test card. The letters and the line designated 20 should be read at 20 feet recording 20/20 vision. When a refractory error is considered, the patient needs to view these letters through a pinhole using a piece of paper and creating a hole of approximately 1 mm. Marked deterioration of vision is recorded using several standard landmarks. For example a vision of 1/60 is present when a patient is able to see finger counting at 1-m distance, 1/200 when moving of the hand is observed. 1/¥ when only light perception is present and zero when completely blind. These abnormalities are typically seen in patients with a lesion of the optic nerve, often due to optic neuritis or anterior ischemic optic neuropathy. The visual fields are tested with a confrontation method in which the patient faces the examiner, covers one eye with his hand, and fixes his gaze on the examiner’s nose. The examiner’s wiggling finger is then brought in along all four quadrants and mentioned by the patient when it comes into view. Visual field defects are named hemianopsia when there is loss of vision in one half field of one eye. Loss vision in corresponding halves of both visual fields is called homonymous hemianopsia. Localization of a homonymous hemianopsia is typically in the occipital cortex. However, macular (central) sparing may occur due to significant collateral branches from the middle cerebral artery. Lesions in the temporal lobe produce a "pie in the sky" homonymous defect. A lesion in the parietal lobe produces a lower quadrant defect. Examination is followed by fundoscopy in which the optic disk is assessed. Dilatation of the pupil is not needed for most purposes but when in doubt a more complete examination with assessment of the macula should follow. Disk swelling is apparent with loss of the normal venous pulse first followed by loss of sharp temporal or nasal margins. Papilledema in advanced forms assumes the configuration of a champagne cork and peripheral hemorrhages are seen. Papilledema indicates increased intracranial pressure from a mass or due to cerebral venous obstruction. It may also seen in a central venous occlusion and may at times be difficult to distinguish from congenital lesions such as a drusen optic disk or anomalous elevation.

The pupil size and reflexes are tested typically in a darkened room. Pupils are normally equal in size, although a 1-mm difference may be physiologic. Bright light will produce constriction except in a blind eye. The differential diagnosis of myosis or mydriasis is shown in Table 4.

When anisocoria is noticed on should determine change in dim or bright light. As a general rule, increase in difference in bright light indicates an abnormality in the sphincter (iris damage, atropine), decrease in bright light indicates iris dilator weakness (Horner syndrome, Adie syndrome, uveitis).

The ocular movements are investigated by having the patient turn the eyes in a horizontal and vertical plane tracking the physician finger. Vertical gaze tends to diminish with age. It is important to record saccades which are "stammering" eye movements often caused by drugs, also degenerative neurologic disorders such as Parkinson’s disease or progressive supranuclear palsy. In addition, convergence is examined. The examination may also be further examined using the optokinetic nystagmus in which the patients look in front of a drum containing a series of lines. Particularly patients with parietal lesions have an abnormal optokinetic nystagmus. Diplopia is difficult to assess but certain rules can be applied. These are the following:

1. The distance between the true and the false image increases with direction of action of the paretic muscle. (In a sixth nerve palsy on the right the images are widest apart when looking to the right.)
2. Horizontal diplopia occurs with lesions of the medial or lateral recti muscles.
3. Vertical diplopia occurs with a superior or inferior recti or oblique muscles. The more peripherally seen image is always the false image.

Nystagmus is noted as well. Typically a nystagmus is a pendular movement in which the movements are of equal velocity. Eye jerk is divided into a fast and slow phase. First degree nystagmus to the right is revealed on a right lateral gaze and shows fast phase to the right. Nystagmus on forward gaze is second degree and on left lateral gaze is called third degree. Nystagmus in the vestibular nucleus is jerk type rotation. The differentiation between a central and peripheral nystagmus is difficult. Central vestibular nystagmus is often vertical, purely torsional and worse looking down and out. In addition vision does not suppress the centrally mediated nystagmus and vertigo is mild. Nystagmus from a central lesion often is part of a symptom complex with other brain stem signs. In some patients a congenital nystagmus is found and is recognized by irregular conjugate, horizontal and in up gaze, accentuated by fixation and anxiety and significantly diminished by convergence.

The trigeminal nerve consists of motor and sensory fibers. The sensory dermatome involves the scalp close to the line of the ear to forehead, eye, cheek, and chin. It can be tested by light touch using a cotton Q-tip, pin, and temperature using hot and cold tubes. The corneal reflex is tested using a cotton ball gently striking the outer rim rather than centrally on the cornea causing a reflective blink. The patient should also indicate touch. In addition, the jaw jerk is elicited by tapping on the apex of the jaw. The response is only significant when it is exaggerated and may indicates a brain stem lesion.

This is tested having the patient elevate eyebrows, closing eyelids forcefully in which the eyelashes disappear, and producing a voluntary smile. When a paralysis of the facial nerve exists, pronounciation of sounds that require closure of the lip such as pot and boy is disturbed. In a peripheral seventh nerve palsy the platysma is also abnormal and can be examined after the patient draws the lower lip and the angle of the mouth downwards. Taste may be abnormal but only when the lesion is peripheral to its junction with the cordae tympany. It is examined using sugar, salt, and sometimes tartaric acid but the results are difficult to interpret. A common peripheral facial paralysis called Bell’s palsy can be recognized by involvement of all three branches, inability to blink and close the eyelid, tearing, and a so-called Bell’s phenomenon in which with forceful closure of the eye the globe turns upward.

Hearing is tested with a whisper voice. The examiner stands in front of the patient and whispers words (e.g. - 66, Boston) while covering patient eyes with one hand and blocking the ear that is not tested with the other hand. Several tuning fork tests are available. The Weber test is a test in which tuning fork is placed in the middle of the skull in which hearing normally should be observed in both ears. Lateralization occurs on the same side in the middle ear involvement, on the opposite side when the cochlear nerve is involved. The Rinne test is performed after placing the vibrating tuning fork against the mastoid and when it can no longer be heard it is held in front of the ear. Positive result is when the tuning fork is heard longer by air than bone conduction. An abnormal test is a sign of middle ear defect or a blocking of the external auditory canal. Vestibular function can be examined with laboratory and caloric testing but also using the Barany test. The patient is seated on examining table and will be reclined backwards with the head hanging over the edge of the table. After a brief interval vertigo will set in and at the same time a brief rotary nystagmus appears. The patient is asked to look downwards. The test is sensitive for a benign positional nystagmus. BPPD is due to dysfunction of the vestibular organ. It is common and often misdiagnosed as vertebral - basilar insufficiency.

This nerve is tested by putting a tongue depressor in the back of the throat which will produce a gag reflex. Midline elevation of the soft palate occurs. Its significance is dubious because many normal individuals have no gag with stimulation.

The patient is asked to say "ah" and the soft palate will rise symmetrically. When there is weakness on one side, deviation will be to the intact side. Swallowing should not be impaired with unilateral involvement of the vagus but hoarseness occurs with involvement of the vocal cord on the affected side.

Accessory nerve is examined by having the patient turn the head forcefully against examiner hand and shrugging both shoulders against resistance. Paralysis of the trapezius muscle or sternocleidomastoid muscle can be observed and often is due to a peripheral nerve damage associated with a lymph biopsy lateral in the neck.

The patient is asked to protrude the tongue and then also the tongue is investigated carefully for atrophy and fasciculations. Tongue fasciculations are strong indicators of ALS in the appropriate setting. It may a appear like a bag of worms. The patient then is asked to rapidly move the tongue from left to right and the strength is tested by pushing the tongue against a tongue blade or against the cheek.

Muscle examination includes inspection for atrophy, fasciculations, and tone. Tone can be rigid or decreased. Typically proximal and distal muscles are tested and are graded using the Medical Research Counsel (MRC) scale.

Muscle atrophy is seen in many diseases of the peripheral nerve but also in advanced myopathies. Generally muscle weakness in myopathies involves muscles in a proximal distribution and peripheral nerve in a distal distribution (hand and foot muscles).

Muscle weakness may involve a nerve root or single nerve. It is summarized in Table 8. Fasciculations are fine twitches in parts of muscle and typically do occur at areas of the limb that the examiner is not looking at ("the shooting star phenomenon"). Muscle tone is assessed after passive movement of the muscle and often muscle tone becomes clear to resistance. Hypotonia is apparent when a limb is shaken by the examiner documenting significant flailing. Loose and toneless muscles not only can be seen in peripheral nerve abnormalities also in the setting of acute cerebellar lesions. Spasticity is diagnosed with increasing resistance to passive movement followed by a sudden release of resistance, typically called a clasp knife reaction.

Tendon reflexes localize to various segments in the spinal cord. The biceps reflex (C5-C6), triceps (C6-C7), knee (L2, L3, and L4), and ankle (L5-S1). Deep tendon reflexes are also classified using a simple grading system (Table 7).

Reflexes in patients may be depressed without any pathological meaning and in many patients voluntary contracting a muscle in other limb will facilitate the reflex (Jendrassik maneuver). Important reflexes are a normal plantar reflex (toes curling down), Babinski sign (unfortunately often called reflex, response or worse "the Babinskis") typically when a piece of metal or wood is applied to lateral surface of the foot or moved in a hockey stick curve from the heel to the front. It results in flexion of the great toe, spreading of the toes in a same response as flexing the knee and contraction of the tensor fascia lata (so called triple response). Other reflexes that need to be examined are abdominal reflexes, stroking the surface of the abdomen in four segments. Contraction is seen, but in elderly obese, and patients with lax abdominal muscles, reflexes are most of the time absent. When the two lowest abdominal responses are absent, a localized spinal cord lesion is at the T10 level. Many other reflexes have been described. They include snout reflex by stimulating the lips, grasp reflex with persistent flexion of the fingers after insertion of two fingers in the palm, palmomental reflex with pressure on the palm causing a contraction of the ipsilateral mentalis muscle, all potentially indicating cortical inhibition. The Hoffmann-Tromner reflex is obtained by snapping the terminal phalanx of the middle finger causing the flexion response of all fingers. The abnormality has been falsely considered "the Babinski of the arm" but only asymmetries are of importance. It is often difficult to elicit.

Sensory testing involves assessment of light touch, pinprick, vibration sense, and joint position sense, and in occasional situations temperature assessment. Light touch involves wisp of cotton ball. The skin is touched, not moved, along it. Pinprick is tested with a sterile pin. Vibration using a tuning fork has similar meaning as joint position sense. Typically movement of the toe up or down is assessed or the patient imitates the same movement in the other limb. When a sensory level is noted by the patient the margins of abnormality needs to be carefully localized. Important pointers are shoulders (C4), nipples (TH4) and navel (TH10). Significant loss of proprioception will cause pseudoathetosis in which the fingers constantly try to orient themselves in space. A 2-point discrimination is also assessing the posterior column and normally stimulus separated by 2 mm should be distinguished.

Cerebellar function is tested with a finger-to-nose test or finger-to-finger test typically using additional turning in the wrists to further test coordination. The most commonly neglected investigation in bed bound patients is a sitting position in which patient may fall to one side with a midline vermis lesion. Dysmetria is noted when the patient cannot smoothly touch the nose and becomes shaky when reaching target.

A favorite pastime of neurologists is to investigate gait. Typically the patient is asked to walk on the hallway and several components are investigated - stability, stride, initiation of gait, and turns. Typical abnormalities in a Parkinson’s patient is stooped gait, reduced arm swing, fragmentary turning. In a patient with a hemiplegia the affected leg is swung outwards with a tendency for the foot to catch on the ground. Profound loss of sensory information from the feet is actually heard due a stamping gait.

This document is not designed to give a complete evaluation of the localization techniques and the reader should be referred to the book by Brazis, Masdeu, and Biller, Localization in Clinical Neurology, Lippincott Raven, 3^rd Edition. Some generalities should be mentioned. Lesions of the upper motor neuron will give paralysis, distally more involved in than the proximal muscles as well as increased reflexes and clonus, and loss of cutaneous reflexes and a Babinski sign. Lesions of the lower motor neuron involve atrophy, flaccid paralysis, fasciculations and weakness is segmental in character. The segmental distribution is noticeable. Specific muscles are innervated through a single cord segment because the spinal cord is arranged through separate reflex arcs. Absence of sensory abnormalities are seen when the lesion is entirely anterior horn. Lesions of the extrapyramidal system will produce bradykinesia with slowness of movement, tremor, shuffling walking with small steps, slow movements, resting tremor, and slowing of mentation as well as initiating movements. Posterior column syndromes involve ataxia, dysmetria with impossibility of coordinated smooth movements, overshooting the mark and increase in symptoms after elimination of vision. Syndromes of cerebellar abnormalities involve decomposition of movement, inability to perform movements smoothly, hypertonia, excessive rebound, and intention tremor.

Alpers and Mancall's Essentials of the Neurological Examination, Edition 2.

Clinical Examination in Neurology Mayo Clinic and Mayo Foundation, 7^th Edition.

Brazis, Masdeu, and Biller. Localization Clinical Neurology, Lippincott and Williams.

Brust. Neurotoxic Side Effects of Prescription Drugs. Butterworth-Heinemann.