Tiburzi Exam 2

Muscle Strength

*****Impaired strength or weakness is called paresis. Absent strength is paralysis, or plegia. Hemiparesis refers to weakness of one half of the body; hemiplegia refers to paralysis of one half of the body. Paraplegia means paralysis of the legs; quadriplegia means paralysis of all four limbs. -Test muscle strength by asking the patient to actively resist your movement. -Remember that a muscle is strongest when shortest, and weakest when lon- gest. Give the patient the advantage as you try to overcome the resistance and judge true the muscle's true strength. -If the muscles are too weak to overcome resistance, test them against gravity alone or with gravity eliminated. When the forearm rests in a pronated position, for example, dorsiflexion at the wrist can be tested against gravity alone. When the forearm is midway between pronation and supination, extension at the wrist can be tested with gravity eliminated. Finally, if the patient fails to move the body part, observe or palpate for weak muscular contraction. **Muscle strength is graded on a 0 to 5 scale: 0 —No muscular contraction detected 1 —A barely detectable flicker or trace of contraction 2 —Active movement of the body part with gravity eliminated 3 —Active movement against gravity 4 —Active movement against gravity and some resistance 5—Active movement against full resistance without evident fatigue. This is normal muscle strength. ****Many clinicians make further distinctions by adding plus or minus signs toward the stronger end of this scale. Thus, 4+ indicates good but not full strength, while 5− means a trace of weakness. -In exam: Test elbow flexion. Testing elbow extension. Test wrist extension. Test grip strength. Test finger abduction. Test opposition of the thumb. Test hip flexion. Test knee extension. Test knee flexion Test ankle dorsiflexion. Testing plantar flexion. Test rapid alternating arm movement. Test rapid finger tapping.

Basic structure of neuro exam

*Mental Status —level of alertness, appropriateness of responses, orientation to date and place *Cranial Nerves ● Vision—visual fields, funduscopic examination ● Pupillary light reflex ● Eye movements ● Hearing ● Facial strength—smile, eye closure *Motor System ● Strength—shoulder abduction, elbow extension, wrist extension, finger abduction, hip flexion, knee flexion, ankle dorsiflexion ● Gait—casual, heel walk, toe walk, tandem walk ● Coordination—fine finger movements, finger-to-nose, heel-knee-shin *Sensory System —one modality at toes—can be light touch, pain/temperature, or proprioception *Reflexes ● Deep tendon reflexes—biceps, patellar, Achilles ● Plantar responses ****Note: If there is reason to suspect neurologic disease based on the patient's his- tory or the results of any components of the screening examination, a more com- plete neurologic examination is necessary.

Lumbosacral radiculopathy: Straight leg raise

*Special technique* -If the patient has low back pain that radiates down the thigh and leg, commonly called sciatica if in the sciatic nerve distribution, test straight-leg raising on each side in turn. Place the patient in the supine position. Raise the patient's relaxed and straight- ened leg, flexing the thigh at the hip. Some examiners first raise the patient's leg with the knee flexed, then extend the leg -Compression of the spinal nerve root as it passes through the vertebral foramen causes a painful radiculopa- thy with associated muscle weakness and dermatomal sensory loss, usually from a herniated disc. -More than 95% of disc herniations occur at L4-L5 or L5-S1, where the spine angles sharply posterior. Look for confirming ipsilateral leg wasting or weak ankle dorsiflexion, which make the diagnosis of sciatica five times more likely. -Assess the degree of elevation at which pain occurs, the quality and distribution of the pain, and the effects of foot dorsiflexion. Tightness or discomfort in the buttocks or hamstrings is common during these maneuvers and should not be interpreted as "radiating pain" or a positive test. *******Pain radiating into the ipsilateral leg is a positive straight leg test for lumbosacral radiculopathy. Foot dorsiflexion can further increase leg pain in lumbosacral radiculopathy, sciatic neuropathy, or both. Increased pain when the contralateral healthy leg is raised is a positive crossed straight-leg raise sign. These maneuvers stretch the affected nerve roots and sciatic nerve. -be sure to examine motor and sensory function and reflexes at the lumbosacral levels.

Tremors or Involuntary Movements

-"a rhythmic oscillatory movement of a body part resulting from the contraction of opposing muscle groups," is the most common movement disorder. -may be an isolated finding or part of a neurologic disorder. -Does the tremor occur at rest? Does it get worse with voluntary intentional movement or with sustained postures? ******Low-frequency unilateral resting tremor, rigidity, and bradykinesia typ- ify Parkinson disease.43,44 Essential tremors are high-frequency, bilateral, upper extremity tremors that occur with both limb movement and sus- tained posture and subside when the limb is relaxed; head, voice, and leg tremor may also be present. -Distinct from these symptoms is restless legs syndrome, present in 6% to 12% of the U.S. population, described as an unpleasant sensation in the legs, especially at night, that gets worse with rest and improves with movement of the symptom- atic limb(s) *****Reversible causes of restless legs syndrome include pregnancy, renal disease, and iron deficiency.

The Brachioradialis Reflex

-(C5, C6). -The patient's hand should rest on the abdomen or the lap, with the forearm partly pronated. Strike the radius with the point or flat edge of the reflex hammer, about 1 to 2 inches above the wrist. Watch for flexion and supination of the forearm.

The Biceps Reflex

-(C5, C6). -The patient's elbow should be partially flexed and the forearm pronated with palm down. Place your thumb or finger firmly on the biceps tendon. Aim the strike with the reflex hammer directly through your digit toward the biceps tendon -Observe flexion at the elbow, and watch for and feel the contraction of the biceps muscle.

The Triceps Reflex

-(C6, C7). -The patient may be sitting or supine. Flex the patient's arm at the elbow, with palm toward the body, and pull it slightly across the chest. Strike the triceps tendon with a direct blow directly behind and just above the elbow. Watch for contraction of the triceps muscle and extension at the elbow. -If you have difficulty getting the patient to relax, try supporting the upper arm. Ask the patient to let the arm go limp, as if it were "hung up to dry." Then strike the triceps tendon

extension at the wrist

-(C6, C7, C8, radial nerve— extensor carpi radialis lon- gus and brevis) -Test extension at the wrist by asking the patient to make a fist and resist as you press down. Or ask the patient to extend the forearms with fingers straight and palms up, then press the palms downward. *****Extensor weakness is seen in periph- eral radial nerve damage, and in the hemiplegia of CNS disease seen in stroke or multiple sclerosis.

Test the grip

-(C7, C8, T1) -Ask the patient to squeeze two of your fingers as hard as possible and not let them go. -To avoid getting hurt by strong grips, place your own middle finger on top of your index finger. Normally it should be difficult for you to pull your fingers from the patient's grip. Test both grips simultaneously with the patient's arms extended or in the lap to help com- pare the right handgrip with the left. *****A weak grip is seen in cervical radicu- lopathy, median or ulnar peripheral nerve disease, and pain from de Quer- vain tenosynovitis, carpal tunnel syn- drome, arthritis, and epicondylitis

Test opposition of the thumb

-(C8, T1, median nerve). -Ask the patient to touch the tip of the little finger with the thumb, against your resistance *****Inspect for weak opposition of the thumb in median nerve disorders such as carpal tunnel syndrome

Test finger abduction

-(C8, T1, ulnar nerve). -Position the patient's hand with palm down and fingers spread. Instruct the patient to prevent you from moving any fingers as you try to force them together ******Weak finger abduction occurs in ulnar nerve disorders.

The Quadriceps (Patellar) Reflex

-(L2, L3, L4). -The patient may be either sitting or lying down as long as the knee is flexed. Briskly tap the patellar tendon just below the patella. -Note contraction of the quadriceps with extension at the knee. Placing your hand on the patient's anterior thigh lets you feel this reflex. -There are two options for examining the supine patient. Supporting both knees at once allows you to assess small differences between quadriceps reflexes by repeatedly testing one reflex and then the other. If supporting both legs is uncomfortable for you or the patient, you can place your supporting arm under the patient's leg. Some patients find it easier to relax with this method.

Test adduction/abduction at the hips

-(L2, L3, L4—adductors). Place your hands firmly on the bed between the patient's knees. Ask the patient to bring both legs together. -Test abduction at the hips (L4, L5, S1—gluteus medius and minimus). Place your hands firmly outside the patient's knees. Ask the patient to spread both legs against your hands. *******Symmetric weakness of the proximal muscles suggests myopathy; symmet- ric weakness of distal muscles sug- gests polyneuropathy, or disorders of peripheral nerves.

flexion at the hip

-(L2, L3, L4—iliopsoas) -by placing your hand on the patient's mid-thigh and asking the patient to raise the leg against your hand

Test extension at the knee

-(L2, L3, L4—quadriceps) -Support the knee in flexion and ask the patient to straighten the leg against your hand. The quadriceps is the strongest muscle in the body, so expect a forceful response.

Test flexion at the knee

-(L4, L5, S1, S2—hamstrings) -Position the patient's leg so that the knee is flexed with the foot resting on the bed. Tell the patient to keep the foot down as you try to straighten the leg

The Achilles (Ankle) Reflex

-(Primarily S1). -If the patient is sitting, partially dorsiflex the foot at the ankle. Persuade the patient to relax. Strike the Achilles tendon, and watch and feel for plantar flexion at the ankle. Also note the speed of relaxation after muscular contraction. ****The slowed relaxation phase of reflexes in hypothyroidism is often best detected during the ankle reflex -When the patient is lying down, flex one leg at both hip and knee and rotate it externally so that the lower leg rests across the opposite shin. Then dorsiflex the foot at the ankle and strike the Achilles tendon

Test extension at the hips

-(S1—gluteus maximus) -Have the patient push the mid posterior thigh down against your hand.

muscle stretch reflexes

-AKA deep tendon reflexes -reflex is an involuntary stereotypical response that may involve as few as two neurons, one afferent (sensory) and one efferent (motor), across a single synapse. The muscle stretch reflexes in the arms and legs are such monosynaptic reflexes. -For a reflex to occur, all components of the reflex arc must be intact: sensory nerve fibers, spinal cord synapse, motor nerve fibers, neuromuscular junction, and muscle fibers. -Tapping the tendon activates special sensory fibers in the partially stretched muscle, triggering a sensory impulse that travels to the spinal cord via a peripheral nerve. The stimulated sensory fiber synapses directly with the anterior horn cell innervating the same muscle. When the impulse crosses the neuromuscular junction, the muscle suddenly contracts, completing the reflex arc. -Because each muscle stretch reflex involves specific spinal segments, together with their sensory and motor fibers, an abnormal reflex helps you locate a pathologic lesion.

Cutaneous Stimulation Reflexes

-Abdominal reflexes *upper : T8, 9, 10 *lower: T10, 11, 12 -Cremasteric reflex: L1, 2 -Plantar responses: L5, S1 -Anal: S2, 3, 4

Muscle Stretch Reflexes and their spinal segments

-Ankle: S1 -Knee: L2, 3, 4 -Supinator (bachioradialis): C5, 6 -Biceps: C5, 6 -Triceps: C6, 7

Point-to-Point Movement

-Arms *Finger-to-Nose Test. Ask the patient to touch your index finger and then his or her nose alternately several times. Move your finger so that the patient has to change directions and extend the arm fully to reach your finger. Observe the accuracy and smoothness of movement, and watch for any tremor. *****In cerebellar disease, movements are clumsy, unsteady, and inappropriately variable in their speed, force, and direction. In dysmetria the patient's fin- ger may initially overshoot the mark, but then reach it fairly well. An inten- tion tremor may appear toward the end of the movement *Now hold your finger in one place so that the patient can touch it with one arm and finger outstretched. Ask the patient to raise the arm overhead and lower it again to touch your finger. After several repeats, ask the patient to close both eyes and try several more times. Repeat on the other side. Normally the patient touches the examiner's finger successfully with eyes open or closed. These maneuvers test position sense and the function of both the labyrinth of the inner ear and the cerebellum. *****In cerebellar disease, incoordination modestly worsens with eyes closed, indicating loss of position sense. Consistent deviation to one side which worsens with the eyes closed, referred to as past pointing, suggests cerebellar or vestibular disease. Legs —Heel-to-Shin Test. Ask the patient to place one heel on the opposite knee, then run it down the shin to the big toe. Observe this movement for smoothness and accuracy. Repetition with the patient's eyes closed tests for position sense. Repeat on the other side. *****In cerebellar disease, the heel may overshoot the knee, then oscillate from side to side down the shin. If position sense is absent, the heel lifts too high and the patient tries to look. With eyes closed, performance is poor.

Rapid Alternating Movements

-Arms. *Show the patient how to strike one hand on the thigh, raise the hand, turn it over, and then strike the back of the hand down on the same place. Urge the patient to repeat these alternating movements as rapidly as possible *Show the patient how to tap the distal joint of the thumb with the tip of the index finger, again as rapidly as possible. Again, observe the speed, rhythm, and smoothness of the movements. The nondominant side often performs less well. *******In cerebellar disease, instead of alter- nating quickly, these movements are slow, irregular, and clumsy, an abnormality called dysdiadochokinesis. Upper motor neuron weakness and basal ganglia disease can also impair these movements, but not in the same manner. -Legs. *Ask the patient to tap the ball of each foot in turn as quickly as possible on your hand or the floor. Note any slowness or awkwardness. Normally the feet do not perform as well as the hands. ******Dysdiadochokinesis points to cerebellar disease.

Gait.

-Ask the patient to: *Walk across the room or down the hall, then turn and come back. Observe posture, balance, swinging of the arms, and movements of the legs. Normally balance is intact, the arms swing symmetrically at the sides, and turns are smooth *****Gait abnormalities increase risk of falls. A uncoordinated gait with reeling and instability is ataxic. Ataxia is seen in cerebellar disease, loss of position sense, and intoxication. *Walk heel-to-toe in a straight line— called tandem walking ******Tandem walking may reveal ataxia that is not otherwise obvious. *Walk on the toes, then on the heels— this tests plantar flexion and dorsiflexion of the ankles as well as balance. ********Walking on toes and heels may reveal distal leg weakness. Inability to heel- walk is a sensitive test for corticospinal tract damage. *Hop in place on each foot in turn (if the patient is not too ill)—this tests proximal and distal muscle strength in the legs and requires both normal position sense and cerebellar function *********Difficulty hopping points to weakness, lack of position sense, or cerebellar dysfunction *Do a shallow knee bend, first on one leg, then on the other. Steady the patient if you think the patient might fall. Or alternatively, rise from a sitting position without arm support and step up on a sturdy stool—if the patient is unsteady, neurologically impaired, or frail these tests are more suitable than hopping or knee bends. *********Difficulty doing shallow knee bends suggests proximal weakness (extensors of the hip), weakness of the quadriceps (extensor of the knee), or both. Proximal muscle weakness in the pel- vic girdle and legs causes difficulty with both of these activities.

The Spinal Cord.

-Below the medulla, the CNS extends into the elongated spinal cord, encased within the bony vertebral column and terminating at the first or second lumbar vertebra -The motor and sensory nerve pathways relay neural signals that enter and exit the cord through posterior and anterior nerve roots and the spinal and peripheral nerves. -cervical, from C1 to C8; thoracic, from T1 to T12; lumbar, from L1 to L5; sacral, from S1 to S5; and coccygeal. The spinal cord is thickest in the cervical segment, which contains nerve tracts to and from both the upper and lower extremities. -Note that the spinal cord is not as long as the vertebral canal. The lumbar and sacral roots travel the longest intraspinal distance and fan out like a horse's tail at L1-L2, giving rise to the term cauda equina. To avoid injury to the spinal cord, most lumbar punctures are performed at the L3-L4 or L4-L5 vertebral interspaces. *Each nerve has an anterior (ventral) root containing motor fibers and a posterior (dorsal) root containing sensory fibers; the anterior and posterior roots merge to form a short (<5 mm) spinal nerve *Spinal nerve fibers commingle with similar fibers from other levels to form peripheral nerves

Feinting/blacking out

-Common and warrant a meticulous history to guide management and possible hospital admission -Begin by finding out whether the patient has actually lost consciousness. Did the patient hear external noise or voices throughout the episode, feel light-headed or weak, but fail to actually lose consciousness, consistent with near syncope or presyncope? Or did the patient actually experience complete loss of consciousness, a more serious symptom representing true syncope, defined as a sudden but temporary loss of consciousness and postural tone from transient global hypoperfusion of the brain? *******Causes include seizures, "neurocardiogenic" conditions such as vasovagal syncope, postural tachycardia syndrome, carotid sinus syncope, and orthostatic hypotension, and cardiac disease causing arrhythmias, especially ventricular tachycardia and bradyarrhythmias. Stroke or sub- arachnoid hemorrhage are unlikely causes of syncope unless both hemispheres are affected. -Elicit a complete description of the event. What was the patient doing when the episode occurred? Was the patient standing, sitting, or lying down? Were there any triggers or warning symptoms? How long did the episode last? Could voices still be heard? Importantly, were onset and offset slow or fast? Were there any palpitations? Is there a history of heart disease, which has a sensitivity for a cardiac cause of more than 95% (with a specificity of ∼45%)? *****In vasovagal syncope, the most common cause of syncope, look for the prodrome of nausea, diaphoresis, and pallor triggered by a fearful or unpleasant event, then vagally mediated hypotension, often with slow onset and offset. In syncope from arrhythmias, onset and offset are often sudden, reflecting loss and recovery of cerebral perfusion. -Try to interview any witnesses. Consider the possibility of a seizure based on the features described in the following section, especially if the onset was abrupt and without warning.

The Anal Reflex.

-Cutaneous/Superficial Stimulation Reflex -Using a broken applicator stick or pinprick, lightly scratch the anus on both sides. Watch for reflex contraction of the external anal sphincter. Detection of the reflex contraction is facilitated by placing a gloved finger in the anus during testing. ********Loss of the anal reflex suggests a lesion in the S2-3-4 reflex arc, seen in cauda equina lesions.

The Plantar Response

-Cutaneous/Superficial Stimulation Reflexe -(L5, S1). -With a key or the wooden end of an applicator stick, stroke the lateral aspect of the sole from the heel to the ball of the foot, curving medially across the ball. Use the lightest stimulus needed to provoke a response, but increase firmness if necessary. Closely observe movement of the big toe, normally plantar flexion. ******Dorsiflexion of the big toe is a positive Babinski response, arising from a CNS lesion affecting the corticospinal tract. The Babinski response can be transiently positive in unconscious states from drug or alcohol intoxication and during the postictal period following a seizure. -Some patients withdraw from this stimulus by flexing the hip and the knee. Hold the ankle, if necessary, to complete your observation. At times it is difficult to distinguish withdrawal from a Babinski response. *******A marked Babinski response is occasionally accompanied by reflex flexion at hip and knee.

The Abdominal Reflexes

-Cutaneous/Superficial Stimulation Reflexes *Test the abdominal reflexes by lightly but briskly stroking each side of the abdomen, above (T8, T9, T10) and below (T10, T11, T12) the umbilicus in 4 outward directions. *Use a key, the wooden end of a cotton-tipped applicator, or a tongue blade twisted and split longitudinally. *Note the contraction of the abdominal muscles and movement of the umbilicus toward the stimulus. If obesity or previous abdominal surgery masks the abdominal reflexes, retract the patient's umbilicus away from the side being tested with your finger and feel for the muscular contraction ******Abdominal reflexes may be absent in both central and peripheral nerve disorders.

Disease of the basal ganglia system or cerebellar system

-Damage to the basal ganglia system produces changes in muscle tone (most often an increase), disturbances in posture and gait, a slow- ness or lack of spontaneous and automatic movements termed bradykinesia, and various involuntary movements -Cerebellar damage impairs coordination, gait, and equilibrium, and decreases muscle tone

Detecting the "Three Ds": Delirium, Dementia, and Depression

-Delirium: acute confusional state marked by sudden onset, fluctuating course, inattention, and at times changing levels of consciousness. --About one third of older adults experience delirium during hospitalizations on medical services; rates are even higher following major elective surgeries. Intensive care unit admissions are associated with a high incidence of delirium regardless of age. Even though delirium is associated with poor patient outcomes, more than 50% of cases are undetected. --The Confusion Assessment Method (CAM) Diagnostic Algorithm: 1. Acute change in mental status and fluctuating course ● Is there evidence of an acute change in cognition from baseline? ● Does the abnormal behavior fluctuate during the day? 2. Inattention ● Does the patient have difficulty focusing attention? 3. Disorganized thinking ● Does the patient have rambling or irrelevant conversations, unclear or illogical flow of ideas, or unpredictable switching from subject to subject? 4. Abnormal level of consciousness ● Is the patient anything besides alert—hyperalert, lethargic, stuporous, or comatose? *Diagnosing delirium requires features 1 and 2 and either 3 or 4. -Dementia: characterized by declines in memory and cognitive ability that interfere with activities of daily living. most common types are Alzheimer disease (affecting 5 million Americans over age 65 years), vascular dementia, Lewy body dementia, and frontotemporal dementia. Diagnosing dementia requires exclusion of delirium and depression. Less than 2% of patients with dementia have potentially reversible causes, such as hypothyroidism, medication side effects, normal pressure hydrocephalus, or major depression. ---A meta-analysis identified potentially modifiable risk factors for developing Alzheimer disease, including physical inactivity, depression, smoking, midlife hypertension, midlife obesity, cognitive inactivity or low educational attainment, and diabetes. Not enough evidence to confirm these. -Depression: more common in individuals with significant medical conditions, including several neurologic disorders—dementia, epilepsy, multiple sclerosis, and Parkinson disease—and is also underdiagnosed. 2 Questions helpful: "Have you been feeling down, depressed, or hopeless (depressed mood)?" and, "Have you felt little interest or pleasure in doing things (anhedonia)?"76 Be sure to assess suicidality and the possibility of bipolar disorder in depressed patients. ****The Mini-Mental State Examination, which takes 7 to 10 minutes to admin- ister, is the best studied

four important questions that govern your neurologic evaluation

-Does the patient have neurologic disease? -If so, what is the localization of the lesion(s)? Are your findings symmetric? If findings are asymmetric or otherwise abnormal, do the causative lesions lie in the central nervous system or the peripheral nervous system? -What is the pathophysiology of the process? -What is the preliminary differential diagnosis? -Whether you conduct a comprehensive or screening examination, organize your thinking into five categories: (1) mental status, speech, and language; (2) CNs; (3) the motor system; (4) the sensory system; and (5) reflexes.

Cranial Nerves IX and X

-Glossopharyngeal and Vagus. *patient's voice. Is it hoarse, or does it have a nasal quality? *****Hoarseness occurs in vocal cord paralysis; nasal voice in paralysis of the palate. *Is there difficulty in swallowing? ******Difficulty swallowing suggests pha- ryngeal or palatal weakness. *Ask the patient to say "ah" or to yawn as you watch the movements of the soft pal- ate and the pharynx. The soft palate normally rises symmetrically, the uvula remains in the midline, and each side of the posterior pharynx moves medially, like a curtain. The slightly curved uvula seen occasionally as a normal variation should not be mistaken for a uvula deviated by a lesion of CN IX or X. ******The palate fails to rise with a bilateral lesion of CN X. In unilateral paralysis, one side of the palate fails to rise and, together with the uvula, is pulled toward the normal side *Warn the patient that you are going to test the gag reflex, which some patients may refuse. This reflex consists of elevation of the tongue and soft palate and constriction of the pharyngeal muscles. Stimulate the back of the throat lightly on each side in turn and observe the gag reflex. This reflex is diminished in many normally healthy people. ******Unilateral absence of this reflex suggests a lesion of CN IX, and perhaps CN X.

Proprioception (Joint Position Sense)

-Grasp the patient's big toe, holding it by its sides between your thumb and index finger, then pull it away from the other toes. This prevents extraneous tactile stimuli from affecting testing. -Demonstrate "up" and "down" as you move the patient's toe clearly upward and downward. Then, with the patient's eyes closed, ask the patient to say "up" or "down" when moving the large toe in a small arc. -Repeat the test several times on each side. If position sense is impaired, move proximally to test the ankle joint. In a similar fashion, test position in the fingers, moving proximally, if indicated, to the metacarpophalangeal joints, wrist, and elbow. ******Loss of position sense, like loss of vibration sense, is seen in tabes dorsalis, multiple sclerosis, or B12 deficiency from posterior column disease, and in diabetic neuropathy.

Cranial Nerve XII

-Hypoglossal. *Listen to the articulation of the patient's words. This depends on CNs V, VII, IX, and X, as well as XII. *Inspect the patient's tongue as it lies on the floor of the mouth. Look for any atrophy or fasciculations. Some coarser restless movements are normal. ******Tongue atrophy and fasciculations are present in amyotrophic lateral sclerosis and past polio. *Then, with the patient's tongue protruded, look for asymmetry, atrophy, or deviation from the midline. Ask the patient to move the tongue from side to side, and note the symmetry of the movement. In ambiguous cases, ask the patient to push the tongue against the inside of each cheek in turn as you palpate externally for strength ******In a unilateral cortical lesion, the pro- truded tongue deviates away from the side of the cortical lesion. In CN XII lesions, the tongue deviates to the weak side.

Reinforcement

-If the patient's reflexes are symmetrically diminished or absent, use reinforcement, a technique involving isometric contraction of other muscles for up to 10 seconds that may increase reflex activity. To reinforce the arm reflexes, for example, ask the patient to clench his or her teeth or to squeeze both knees together. If leg reflexes are diminished or absent, ask the patient to lock fingers and pull one hand against the other. Tell the patient to pull just before you strike the patellar or Achilles tendon

Clonus.

-If the reflexes seem hyperactive, test for ankle clonus. -Support the knee in a partly flexed position. With your other hand, dorsiflex and plantar flex the foot a few times while encouraging the patient to relax, then sharply dorsiflex the foot and maintain it in dorsiflexion. Look and feel for rhythmic oscillations between dorsiflexion and plantar flexion. Normally the ankle does not react to this stimulus. There may be a few clonic beats if the patient is tense or has exercised. ******Sustained clonus points to CNS dis- ease. The ankle plantar flexes and dorsiflexes repetitively and rhythmically. Clonus must be present for a reflex to be graded 4 -Other joints may display clonus. A sharp downward displacement of the patella, for example, may elicit patellar clonus in the extended knee

Cranial nerves II and III

-Inspect the size and shape of the pupils, and compare one side with the other. Anisocoria, or a difference of >0.4 mm in the diameter of one pupil compared to the other, is seen in up to 38% of healthy individuals. Test the pupillary reactions to light. ****If the large pupil reacts poorly to light or anisocoria worsens in light, the large pupil has abnormal pupillary constriction, seen in CN III palsy. If ptosis and ophthalmoplegia are also present, consider intracranial aneurysm if the patient is awake, and transtentorial herniation if the patient is comatose. -Also check the near response, which tests pupillary constriction (pupillary constrictor muscle), convergence (medial rectus muscles), and accommodation of the lens (ciliary muscle). *****If both pupils react to light and anisocoria worsens in darkness, the small pupil has abnormal pupillary dilation, seen in Horner syndrome and simple anisocoria

Dermatomes

-Knowledge of dermatomes helps you localize neurologic lesions to a specific level of the spinal cord, particularly in spinal cord injury -Dermatome levels are more variable than these diagrams suggest. They overlap at their upper and lower margins and also slightly across the midline. ******In spinal cord injury, the sensory level may be several segments lower than the spinal lesion, for reasons that are not well understood. Percussing for the level of vertebral pain may be helpful. -T4: nipple -T10: umbilicus -L1: Inguinal -C6: Thumb and side of pointer -C8: Pinky and half of ring fingers -L4: Knee -S5: anus

Light touch/vibration

-Light Touch: With a fine wisp of cotton, touch the skin lightly, avoiding pressure. Ask the patient to respond whenever a touch is felt, and to compare one area with another. Avoid testing calloused skin, which is normally relatively insensitive. ****Anesthesia is absence of touch sensation, hypesthesia is decreased sensitivity to touch, and hyperesthesia is increased sensitivity. -Vibration: Use a relatively low-pitched tuning fork of 128 Hz. Tap it on the heel of your hand and place it firmly over a distal interphalangeal joint of the patient's finger, then over the interphalangeal joint of the big toe. Ask what the patient feels. If you are not sure whether the patient is feeling pressure or vibration, ask the patient to tell you when the vibration stops. Then touch the tuning fork to stop it from vibrating and confirm this change with the patient. If vibration sense is impaired, proceed to more proximal bony prominences (e.g., wrist, elbow; medial malleolus, shin, patella, anterior superior iliac spine, spinous processes, and clavicles). ******Vibration sense is often the first sensation lost in a peripheral neuropathy and increases the likelihood of peripheral neuropathy 16-fold. Causes include diabetes, alcoholism, and posterior column disease, seen in tertiary syphilis or vitamin B12 deficiency. ******Testing vibration sense in the trunk is useful when identifying the level of a cord lesion.

Reducing Risk of Diabetic Peripheral Neuropathy

-Maintaining optimal glycemic control can prevent or delay the onset of neuropathy, particularly from type I diabetes -Distal symmetric sensorimotor polyneuropathy: This is the most common type of diabetic neuropathy. It is slowly progressive, often asymptomatic, and a risk factor for ulcerations, arthropathy, and amputation. Symptomatic patients report burning electrical pain in the lower extremities, usually at night. -Autonomic dysfunction, mononeuropathies, and polyradiculopathies, including diabetic amyotrophy, which initially causes unilateral thigh pain and proximal lower extremity weakness. -Diabetic patients should have their feet examined regularly for neuropathy, including testing pin- prick sensation, ankle reflexes, vibration perception (with a 128-Hz tuning fork) and plantar light touch sensation (with a Semmes-Weinstein mono- filament), as well as checking for skin breakdown, poor circulation, and musculoskeletal abnormalities. The monofilament test involves pressing the perpendicular monofilament against the skin at the great toe and metatarsals until it bends, or against the dorsal arch if without calluses; the test is positive if the patient cannot feel the monofilament.

Lesion at Cerebral Cortex

-Motor: Chronic contralateral corticospinal-type weakness and spasticity; flexion is stronger than extension in the arm, plantar flexion is stronger than dorsiflexion in the foot, and the leg is externally rotated at the hip -Sensory: Contralateral sensory loss in the face, limbs, and trunk on the same side as the motor deficits -Increases deep tendon reflexes -Ex. of cause: Cortical stroke

Lesions at Neuromuscular Junction

-Motor: Fatigability more than weakness -Sensory: Sensation intact -Deep tendon reflexes normal -Causes: myasthenia gravis

Cerebellar lesions

-Motor: Hypotonia, ataxia, nystagmus, dysdiadochokinesis, and dysmetria -Sensory: Not affected -Deep tendon reflexes are normal or decreased -Ex of causes: Cerebellar stroke, brain tumor

Lesions in Subcortical Gray Matter: Basal Ganglia

-Motor: Slowness of movement (bradykinesia), rigidity, and tremor -Sensory: Not affected -Normal or decreased deep tendon reflexes -Ex of causes: Parkinsonism

Lesion in Peripheral Nerve— Mononeuropathy

-Motor: Weakness and atrophy in a peripheral nerve distribution; sometimes with fasciculations -Sensory: Sensory loss in the pattern of that nerve -Decreased deep tendon reflexes -Causes: Trauma

Lesions on Spinal Roots and Nerves

-Motor: Weakness and atrophy in a root- innervated pattern; sometimes with fasciculations -Sensory: Corresponding dermatomal sensory deficits -Deep tendon reflexes are decreased -Causes: Herniated cervical or lumbar disc

Lesions on Anterior Horn Cell

-Motor: Weakness and atrophy in a segmental or focal pattern; fasciculations -Sensory: Intact -Decreased deep tendon reflexes -Ex of causes: Polio, amyotrophic lateral sclerosis

Peripheral Nerve— Polyneuropathy

-Motor: Weakness and atrophy more distal than proximal; sometimes with fasciculations -Sensory: Sensory deficits, commonly in stocking-glove distribution -Decreased deep tendon reflexes -Causes: Peripheral poly- neuropathy of alcoholism, diabetes

Lesions on spinal cord

-Motor: Weakness and spasticity, but often affecting both sides (when cord damage is bilateral), causing paraparesis or quadriparesis depending on the level of injury -Sensory: Dermatomal sensory deficit on the trunk on one or both sides at the level of the lesion, and sensory loss from tract damage below the level of the lesion -Increased deep tendon reflexes -Possible causes: Trauma, spinal cord tumor

Lesions on brainstem

-Motor: Weakness and spasticity, plus CN deficits such as diplopia (from weakness of the extraocular muscles) and dysarthria -Sensory: Variable; no typical sensory findings -increase of deep tendon reflexes -Possible causes: Brainstem stroke, acoustic neuroma

Lesions in muscle

-Motor: Weakness usually more proximal than distal; fasciculations rare -Sensory: Sensation intact -Deep tendon reflexes decreased or normal -Causes: Muscular dystrophy

Cranial Nerves III, IV, and VI

-Oculomotor, Trochlear, and Abducens. *Test the extraocular movements in the six cardinal directions of gaze, and look for loss of conjugate movements in any of the six directions, which causes diplopia. Ask the patient which direction makes the diplopia worse and inspect the eye closely for asymmetric deviation of movement. Determine if the diplo- pia is monocular or binocular by asking the patient to cover one eye, then the other. *****Monocular diplopia is seen in local problems with glasses or contact lenses, cataracts, astigmatism, or ptosis. Binocular diplopia occurs in CN III, IV, and VI neuropathy (40% of patients), and eye muscle disorders from myasthenia gravis, trauma, thyroid ophthalmopathy, and internuclear ophthalmoplegia *Check convergence of the eyes. *Identify any nystagmus, an involuntary jerking movement of the eyes with quick and slow components. Note the direction of gaze in which it appears, the plane of the nystagmus (horizontal, vertical, rotary, or mixed), and the direction of the quick and slow components. Nystagmus is named for the direction of the quick component. Ask the patient to fix his or her vision on a distant object and observe if the nystagmus increases or decreases. *****Nystagmus is seen in cerebellar disease, especially with gait ataxia and dysarthria (increases with retinal fixa- tion), and vestibular disorders (decreases with retinal fixation); and in internuclear ophthalmoplegia. -Look for ptosis (drooping of the upper eyelids). A slight difference in the width of the palpebral fissures is a normal variant in approximately one third of patients. *****Ptosis is seen in 3rd nerve palsy (CN III), Horner syndrome (ptosis, miosis, forehead anhidrosis), or myasthenia gravis.

Cranial Nerve I

-Olfactory. *Test the sense of smell by presenting the patient with familiar nonirritating odors. *First, make sure that each nasal passage is patent by compressing one side of the nose and asking the patient to sniff through the other. Then ask the patient to close both eyes. Occlude one nostril and test smell in the other with substances like cloves, coffee, soap, or vanilla. *Avoid noxious odors like ammonia that might stimulate CN V. Ask the patient to identify each odor. ****Loss of smell occurs in sinus condi- tio ns, head trauma, smoking, aging, use of cocaine, and Parkinson disease.

Cranial Nerve II

-Optic. *Test visual acuity. *Inspect the optic fundi with your ophthalmoscope, paying special attention to the optic discs. *****Inspect each disc carefully for bulging and blurred margins (papilledema); pallor (optic atrophy); and cup enlargement (glaucoma). *Test the visual fields by confrontation. Test each eye separately, and both eyes together. Occasionally, in stroke patients, for example, patients will complain of partial loss of vision, and testing of both eyes reveals a visual field defect, an abnormality in peripheral vision such as homonymous hemianopsia. Testing only one eye would miss this finding. ****Look for prechiasmal, or anterior, defects seen in glaucoma, retinal emboli, optic neuritis (visual acuity poor); bitemporal hemianopsias from defects at the optic chiasm, usually from pituitary tumor; and homony- mous hemianopsias or quadrantanopsias in postchiasmal lesions, usually in the occipital or parietal lobe, with associated findings of stroke (visual acuity normal).

Seizures.

-Patients may report "spells" or fainting that raises suspicion of seizure, a sudden excessive electrical discharge from cortical neurons. Seizures may be symptomatic, with an identifiable cause, or idiopathic -If there is more than one seizure, consider epilepsy, defined as two or more sei- zures that are not provoked by other illnesses or circumstances. ******Common causes of acute symptomatic seizures include: head trauma; alcohol, cocaine, and other drugs; withdrawal from alcohol, benzodiazepines, and barbiturates; metabolic insults from low or high glucose or low calcium or sodium; acute stroke; and meningitis or encephalitis -Epilepsy does not always involve loss of consciousness, depending on the type. -It is usually classified as generalized or partial, based on the location in the cortex of the initial seizure focus. If available, ask a witness how the patient looked before, during, and after the episode. Was there any seizure-like movement of the arms or legs? Any incontinence of the bladder or bowel? What about any drowsiness or impaired memory after the event suggestive of a postictal state? ******Tonic-clonic motor activity, bladder or bowel incontinence, and postictal state characterize generalized sei- zures. Unlike syncope, tongue biting or bruising of limbs may occur. *******Epilepsy is more common in infants and older adults. The baseline neurologic examination is frequently normal. -Ask about age at onset, frequency, change in frequency or symptom pattern, and use of medications, alcohol, or illicit drugs. Check for any history of head injury. ******Generalized epilepsy syndromes usually begin in childhood or adolescence; adult-onset seizures are usually partial.

Preventing Stroke and Transient Ischemic Attack.

-Primary Prevention: *stroke and coronary heart disease share common cardiovascular risk factors and threats to health *Optimal blood pressure control is essential for preventing hemorrhagic stroke. Additional risk factors for the most common cause of hemorrhagic stroke— ruptured aneurysms in the circle of Willis—include smoking, alcohol use, oral contraceptives, and family history in a first-degree relative. -Hypertension is the leading risk factor for both ischemic and hemorrhagic stroke. Pharmacologic reduction of blood pres- sure significantly reduces stroke risk, particularly among Afri- can Americans and older adults. -Smoking is associated with doubling the risk of ischemic stroke -Dyslipedemia: Statin treatment reduces the risk of all strokes by about 20% for patients with or at risk for atherosclerotic cardiovascular disease. -Stroke risk is doubled with diabetes and 20% of diabetic patients will die of stroke. -Obesity increases the risk of ischemic stroke by 64%. Dietary factors affect stroke risk primarily by elevating blood pressure. Decreasing salt and saturated fat intake and diets emphasizing fruits, vegetables, nuts, and low-fat dairy prod- ucts may reduce stroke risk. -Disease-Specific Risk Factors: A-fib (Antiplatelet agents and anticoagulants can reduce the risk for ischemic stroke.), Carotid artery disease, Obstructive sleep apnea -Screening for Asymptomatic Carotid Artery Stenosis. -TIA and Stroke—Secondary Prevention: focus on: identifying the underlying cause including noncardiac emboli, cardiac emboli, and carotid artery stenosis; reducing cardiovascular risk factors, including inactivity, hyperlipidemia, poorly controlled diabetes or hypertension, smoking, and heavy alcohol consumption; and identifying the most appropriate interventions for secondary prevention including antiplatelet agents, anticoagulants, and carotid revascularization. -Strokes in young adults often have a different set of causes—patent foramen ovale and less commonly, carotid or vertebral/basilar artery dissection, hyper- coagulable states, or cocaine and illicit drug use

Muscle Stretch Reflexes

-Reflex hammer: pointed end is useful for striking small areas, such as your finger as it overlies the biceps tendon. -Test the reflexes: Encourage the patient to relax, then position the limbs properly and symmetrically. Hold the reflex hammer loosely between your thumb and index finger so that it swings freely in an arc within the limits set by your palm and other fingers ■ With your wrist relaxed, strike the tendon briskly using a rapid wrist movement. Your strike should be quick and direct, not glancing. -Note the speed, force, and amplitude of the reflex response and grade the response. Always compare the response of one side with the other. Reflexes are usually graded on a 0 to 4 scale. -Reflex response depends partly on the force of your strike on the tendon. Use only enough force to provoke a definite response. Differences between sides are usually easier to detect than symmetric changes on both sides. Symmetrically increased, diminished, or even absent reflexes can be normal.

Discriminative Sensations

-Several additional techniques test the ability of the sensory cortex to correlate, analyze, and interpret sensations. Because discriminative sensations depend on touch and position sense, they are useful only when these sensations are either intact or only slightly impaired. ******If touch and position sense are normal, decreased or absent discriminative sensation indicates a lesion in the sensory cortex. Stereognosis, number identification, and two-point discrimination are also impaired in posterior column disease. -Screen a patient with stereognosis, and proceed to other methods, if indicated. The patient's eyes should be closed during all these tests -Stereognosis: Stereognosis refers to the ability to identify an object by feeling it. Place a familiar object such as a coin, paper clip, key, pen- cil, or cotton ball, in the patient's hand and ask the patient to tell you what it is. Normally a patient will manipulate it skillfully and identify it correctly within 5 seconds. Asking the patient to distinguish "heads" from "tails" on a coin is a sensitive test of stereognosis. *****Astereognosis refers to the inability to recognize objects placed in the hand. -Number identification (graphesthesia): If arthritis or other conditions pre- vent the patient from manipulating an object well enough to identify it, test the ability to identify numbers. With the blunt end of a pen or pencil, draw a large number in the pa- tient's palm. A normally abled person can identify most such numbers. *****The inability to recognize numbers, or graphanesthesia, indicates a lesion in the sensory cortex. -Two-point discrimination: Using the two ends of an opened paper clip, or two pins, touch a finger pad in two places simultaneously. Alternate the double stimulus irregularly with a one-point touch. Be careful not to cause pain. Find the minimal distance at which the patient can discriminate one from two points (normally <5 mm on the finger pads). This test may be used on other parts of the body, but normal distances vary widely from one body region to another. ******Lesions of the sensory cortex increase the distance between two recognizable points. -Point localization: Briefly touch a point on the patient's skin. Then ask the patient to open both eyes and point to the place touched. Normally a person can do so accurately. ******Lesions of the sensory cortex impair the ability to localize points accurately. -Extinction: Stimulate one side or simultaneously stimulate corresponding areas on both sides of the body. Ask where the patient feels your touch. Nor- mally both stimuli are felt. ******With lesions of the sensory cortex, only one stimulus may be recognized. The stimulus to the side opposite the damaged cortex is extinguished.

Meningeal Signs

-Special techniques -Test for these important signs whenever you suspect meningeal inflammation from meningitis or subarachnoid hemorrhage. *****Inflammation in the subarachnoid space causes resistance to movement that stretches the spinal nerves (neck flexion), the femoral nerve (Brudzinski sign), and the sciatic nerve (Kernig sign). -Neck Mobility/Nuchal Rigidity *First, make sure there is no injury or fracture to the cervical vertebrae or cervical cord. In trauma settings, this often requires radiologic evaluation. Then, with the patient supine, place your hands behind the patient's head and flex the neck forward, if possible until the chin touches the chest. Normally the neck is supple, and the patient can easily bend the head and neck forward. *******Neck stiffness with resistance to flex- ion is found in ∼84% of patients with acute bacterial meningitis and 21% to 86% of patients with subarachnoid hemorrhage. It is most reliably present in severe meningeal inflammation but its overall diagnostic accuracy is low. -Budzinski sign: *As you flex the neck, watch the hips and knees in reaction to your maneuver. Normally they should remain relaxed and motionless. *****Flexion of both the hips and knees is a positive Brudzinski sign. -Kernig Sign: *Flex the patient's leg at both the hip and the knee, and then slowly extend the leg and straighten the knee. Discomfort behind the knee during full extension is normal but should not produce pain. *******Pain and increased resistance to knee extension are a positive Kernig sign *******The mechanism of this sign is similar to the positive straight leg raise test. Irritation or compression of a lumbar or sacral nerve root or the sciatic nerve causes radicular or sciatic pain radiating into the leg when the nerve is stretched by extending the leg. ********The frequency of Brudzinski and Kernig signs in patients with meningitis has a reported range of 5% to 60%.

Cranial Nerve XI

-Spinal Accessory. *Standing behind the patient, look for atrophy or fasciculations in the trapezius muscles, and compare one side with the other. Fasciculations are fine flickering irregular movements in small groups of muscle fibers. Ask the patient to shrug both shoulders upward against your hands. Note the strength and contraction of the trapezii. ******Trapezius weakness with atrophy and fasciculations points to a peripheral nerve disorder. In trapezius muscle paralysis, the shoulder droops, and the scapula is displaced downward and laterally. *Ask the patient to turn his or her head to each side against your hand. Observe the contraction of the opposite sternocleido- mastoid (SCM) muscle and note the force of the movement against your hand. ******A supine patient with bilateral weak- ness of the SCM muscles has difficulty raising the head off the pillow.

Stroke fax

-Stroke is a sudden neurologic deficit caused by cerebrovascular ischemia (87%) or hemorrhage (13%). Hemorrhagic strokes may be intracerebral (10% of all strokes) or subarachnoid (3% of all strokes). -TIAs are a major risk factor for stroke, which occurs in 3% to 10% of patients within 2 days and in 9% to 17% within 90 days.47 Short-term stroke risk is high- est in those with age 60 years and older, diabetes, focal symptoms of weakness or impaired speech, and a TIA lasting more than 10 minutes. -Stroke prevalence and mortality are disproportionately higher in African Americans compared to whites: -Although younger and middle-aged women have lower age-specific stroke incidence rates than men, rates increase with age so that women, who on average live longer than men, have an overall higher lifetime risk for stroke. Risk factors for women include autoimmune collagen vascular disease and history of preeclampsia, gestational diabetes, and pregnancy-induced hyper- tension -Stroke outcomes improve significantly when thrombolytic therapy is given within 3 to 4.5 hours of symptom onset; however, only a minority of those suffering a stroke reaches an emergency room within this time window. -The prevalence of silent stroke, estimated to range from 6% to 28%, increases with age. -The most common cause of ischemic symptoms is occlusion of the mid- dle cerebral artery, which causes visual field cuts and contralateral hemiparesis and sensory deficits. Occlusion of the left middle cerebral artery often pro- duces aphasia; and occlusion of the right middle cerebral artery, neglect or inattention to the opposite side of the body. -Stroke Warning Signs: F Face Drooping—Does one side of the face droop or is it numb?53 Ask the per- son to smile. Is the person's smile uneven? A Arm Weakness—Is one arm weak or numb? Ask the person to raise both arms. Does one arm drift downward? S Speech Difficulty—Is speech slurred? Is the person unable to speak or hard to understand? Ask the person to repeat a simple sentence, like "The sky is blue." Is the sentence repeated correctly? T Time to call 9-1-1—If someone shows any of these symptoms, even if the symptoms go away, call 9-1-1 and get the person to the hospital immediately. Check the time so you'll know when the first symptoms appeared -Beyond FAST: Other important symptoms ● Sudden numbness or weakness of the leg, arm, or face ● Sudden confusion or trouble understanding ● Sudden trouble seeing in one or both eyes ● Sudden trouble walking, dizziness, loss of balance or coordination ● Sudden severe headache with no known cause

Testing flexion/extension of elbow

-Test flexion (C5, C6—biceps and brachioradialis) and extension (C6, C7, C8—tri- ceps) at the elbow by having the patient pull and push against your hand

The Brain

-The brain has four regions: the cerebrum, the diencephalon, the brainstem, and the cerebellum. Each cerebral hemisphere is subdivided into frontal, parietal, temporal, and occipital lobes. -Gray matter consists of aggregations of neuronal cell bodies. It rims the surfaces of the cerebral hemispheres, forming the cerebral cortex. White matter consists of neuronal axons that are coated with myelin. The myelin sheaths, which create the white color, allow nerve impulses to travel more rapidly -Deep in the brain lie additional clusters of gray matter These include: *basal ganglia: affect movement *thalamus and the hypothalamus structures in the diencephalon: The thalamus processes sensory impulses and relays them to the cerebral cortex. The hypothalamus maintains homeostasis and regulates temperature, heart rate, and blood pressure. The hypothalamus affects the endocrine system and governs emotional behaviors such as anger and sexual drive. Hormones secreted in the hypothalamus act directly on the pituitary gland. *The internal capsule: a white-matter structure where myelinated fibers converge from all parts of the cerebral cortex and descend into the brainstem *The brainstem: connects the upper part of the brain with the spinal cord, has three sections: the midbrain, the pons, and the medulla. -Consciousness relies on the interaction between intact cerebral hemispheres and a structure in the diencephalon and upper brainstem, the reticular activating (arousal) system. -cerebellum: which lies at the base of the brain, coordinates all movement and helps maintain the body upright in space.

cerebellar system

-The cerebellum receives both sensory and motor input and coordinates motor activity, maintains equilibrium, and helps to control posture.

basal ganglia system

-This exceedingly complex system includes motor pathways between the cerebral cortex, basal ganglia, brainstem, and spinal cord. It helps to maintain muscle tone and to control body movements, especially gross automatic movements such as walking.

Cranial Nerve V

-Trigeminal *Motor: While palpating the temporal and masseter muscles in turn, ask the patient to firmly clench the teeth. Note the strength of muscle contraction. Ask the patient to open and move the jaw from side to side. ****Difficulty clenching the jaw or moving it to the opposite side suggests mas- seter and lateral pterygoid weakness, respectively. Jaw deviation during opening points to weakness on the deviating side. *****Look for unilateral weakness in CN V pontine lesions; bilateral weakness in bilateral hemispheric disease. *****CNS patterns from stroke include ipsi- lateral facial and body sensory loss from contralateral cortical or thalamic lesions; ipsilateral face, but contralat- eral body sensory loss in brainstem lesions. -Sensory: *After explaining what you plan to do, test the forehead, cheeks, and chin on each side for pain sensation in the circled areas in. The patient's eyes should be closed. Use a suitable sharp object such as a pin or cotton swab. You can create a sharp wood splinter by breaking or twisting a cotton swab. To avoid transmit- ting infection, use a new object for each patient. While testing, occasionally substitute the blunt end for the point as a contrasting stimulus. Ask the patient to report whether each stimulus is "sharp" or "dull" and to compare sides *****Isolated sensory loss occurs in peripheral nerve disorders, including lesions of the trigeminal nerve (CN V). *If you detect sensory loss, confirm it by testing temperature sensation. Two test tubes, filled with hot and ice-cold water, are the traditional stimuli. You can also use a tuning fork, which usually feels cool, and make it warm or cool with run- ning water. Dry it, then touch the skin and ask the patient to identify "hot" or "cold." *Then test for light touch, using a fine wisp of cotton. Ask the patient to respond whenever you touch the skin. *Corneal Reflex. Test the corneal reflex. Ask the patient to look up and away from you and approach from the opposite side, out of the patient's line of vision. Avoiding the eyelashes, lightly touch the cornea (not just the conjunctiva) with a fine wisp of cotton. If the patient is apprehensive touching the conjunctiva first may be helpful. Inspect for blinking of both eyes, the normal reaction to this stimulus. The sensory limb of this reflex is carried in CN V, and the motor response in CN VII on both sides. Contact lenses interfere with this testing. *****Blinking is absent in both eyes in CN V lesions and on the side of weakness in lesions of CN VII. Absent blinking and sensorineural hearing loss occur in acoustic neuroma.

The Cranial Nerves.

-Twelve pairs of special nerves called cranial nerves (CNs) emerge from the cranial vault through skull foramina and canals to structures in the head and neck. -They are numbered sequentially with Roman numerals in rostral to caudal order as they arise from the brain. CNs III through XII arise from the diencephalon and the brainstem, CNs I and II are actually fiber tracts emerging from the brain. Some CNs are limited to general motor and/or sensory functions, whereas others are specialized, serving smell, vision, or hearing (I, II, VIII).

Pain/Temp

-Use a sharp safety pin, the stick portion of a broken cotton swab, or other suitable tool. Occasionally, substitute the blunt end for the point. Ask the patient, "Is this sharp or dull?" or, when making comparisons, "Does this feel the same as this?" Apply the lightest pressure needed for the stimulus to feel sharp; avoid heavy pricks that draw blood. -To prevent transmitting a bloodborne infection, discard the pin or other device safely. Do not reuse it on another person. *****Analgesia refers to absence of pain sensation, hypalgesia refers to decreased sensitivity to pain, and hyperalgesia refers to increased pain sensitivity Temperature: Testing skin temperature is often omitted if pain sensation is normal. If there are sensory deficits, use two test tubes filled with hot and cold water, or a tuning fork heated or cooled by running water. Touch the skin and ask the patient to identify "hot" or "cold."

Cranial nerve VIII

-Vestibulocochlear/acoustic *Assess hearing with the whispered voice test. Ask the patient to repeat numbers whispered into one ear while blocking or rubbing your fingers next to the contralateral ear. *****The whispered voice test is both sen- sitive (>90%) and specific (>80%) when assessing presence or absence of hearing loss. *If hearing loss is present, determine if the loss is conductive, from impaired "air through ear" transmission, or sensorineural, from damage to the cochlear branch of CN VIII. Test for air and bone conduction, using the Rinne test, and lateraliza- tion, using the Weber test. *****Excess cerumen, otosclerosis, and oti- tis media cause conductive hearing loss; presbyacusis from aging is usually from sensorineural hearing loss. *****Vertigo with hearing loss and nystag- mus typifies Ménière disease

Damage to the lower motor neuron systems

-causes ipsilateral weakness and paralysis, but in this case, muscle tone and reflexes are decreased or absent.

Dizziness or Vertigo

-common, somewhat vague, complaints that prompt a more specific history and neurologic examination, with emphasis on detection of nystagmus and focal neurologic signs. Especially in older patients, ask about medications. -Does the patient feel faint or about to fall or pass out (presyncope). *****Feeling light-headed, weak in the legs, or about to faint points to pre- syncope from vasovagal stimulation, orthostatic hypotension, arrhythmia, or side effects from blood pressure and other medications. -unsteady and off balance (disequilibrium or ataxia)? -is there true vertigo, a spinning sensation within the patient or of the surroundings? If there is true vertigo, establish the time course of symptoms, which helps distinguish among the different types of peripheral vestibular disorders. ****Vertigo often reflects vestibular disease, usually from peripheral causes in the inner ear such as benign posi- tional vertigo, labyrinthitis, or Ménière disease. -If there are localizing symptoms or signs like double vision (diplopia), difficulty forming words (dysarthria), or problems with gait or balance (ataxia), investigate the central causes of vertigo. *****Ataxia, diplopia, and dysarthria are suspicious for vertebrobasilar TIA or stroke. Also consider posterior fossa tumor and migraine with brainstem aura.

Motor Pathways

-complex avenues that extend from upper motor neurons through long white matter tracts to synapses with lower motor neurons, and continue to the periphery through peripheral nerve structures. -Upper motor neurons, or nerve cell bodies, lie in the motor strip of the cerebral cortex and in several brainstem nuclei; their axons synapse with motor nuclei in the brainstem (for CNs) and in the spinal cord (for peripheral nerves) -Lower motor neurons have cell bodies in the spinal cord, termed anterior horn cells; their axons trans- mit impulses through the anterior roots and spinal nerves into peripheral nerves, terminating at the neuromuscular junction. -Three kinds of motor pathways impinge on the anterior horn cells: the corticospinal tract, the basal ganglia system, and the cerebellar system. Additional pathways originating in the brainstem mediate flexor and extensor tone in limb movement and posture, most notably in coma -All of these higher motor pathways affect movement only through the lower motor neuron systems, sometimes called the "final common pathway." Any move- ment, whether initiated voluntarily in the cortex, "automatically" in the basal gan- glia, or reflexly via the sensory receptors, must ultimately be translated into action by the anterior horn cells. A lesion in any of these areas will affect movement or reflex activity.

spino-thalamic tract

-consisting of smaller sensory neurons with unmyelinated or thinly myelinated axons -The peripheral component of the small- fiber spinothalamic tract arises in free nerve endings in the skin that register pain, tem- perature, and crude touch. -Within one or two spinal segments from their entry into the cord, these fibers pass into the posterior horn and synapse with secondary neurons. The secondary neurons then cross to the opposite side and pass upward into the thalamus.

Peripheral Nervous System

-consists of both CNs and periph- eral nerves that project to the heart, visceral organs, skin, and limbs. -controls the somatic nervous system, which regulates muscle movements and response to the sensations of touch and pain, and the autonomic nervous system that connects to internal organs and gener- ates autonomic reflex responses. The autonomic nervous system consists of the sympathetic nervous system, which "mobilizes organs and their functions during times of stress and arousal, and the para- sympathetic nervous system, which conserves energy and resources during times of rest and relaxation

corticospinal (pyramidal) tract.

-corticospinal tracts mediate voluntary movement and integrate skilled, complicated, or delicate movements by stimulating selected muscular actions and inhibiting others. They also carry impulses that inhibit muscle tone, the slight tension maintained by normal muscle even when it is relaxed. -The corticospinal tracts originate in the motor cortex of the brain Motor fibers travel down into the lower medulla, where they form an anatomical structure resembling a pyramid. There, most of these fibers cross to the opposite or contralateral side of the medulla, continue downward, and synapse with anterior horn cells or with intermediate neurons. Tracts synapsing in the brainstem with motor nuclei of the CNs are termed corticobulbar.

Dermatomes:

-dermatome is the band of skin innervated by the sensory root of a single spinal nerve -Lateral portion of pinky is 8, one of most pure sensory dermatome is there, C6 is thumb -L4 is knee -T10 is umbilicus -L1 is inguinal -T4 is nipples

Test foot dorsiflexion/plantar flexion

-dorsiflex: (mainly L4, L5—tibialis anterior) -Plantar: (mainly S1—gastrocnemius, soleus) at the ankle by asking the patient to pull up and push down against your hand. -Heel and toe walk also assess foot dorsiflexion and plantar flexion, respectively.

The Motor System

-focus on body position, involuntary movements, characteristics of the muscles (bulk, tone, and strength), and coordination. -If you detect an abnormality, identify the muscle(s) involved and if it is central or peripheral in origin. -Body Position. Observe the patient's body position during movement and at rest. *****Abnormal positions alert you to conditions such as mono- or hemiparesis from stroke. -Involuntary Movements. Watch for involuntary movements such as tremors, tics, chorea, or fasciculations. Note their location, quality, rate, rhythm, and amplitude, and their relation to posture, activity, fatigue, emotion, and other factors. ***** -Muscle Bulk: Inspect the size and contours of muscles. Do the muscles look flat or concave, suggesting loss of muscle bulk from atrophy or wasting? If so, is the process unilateral or bilateral? . . . proximal or distal? ******Atrophy results from PNS disorders such as diabetic neuropathy and dis- eases of the muscles themselves. Hypertrophy is an increase in bulk with normal or increased strength; increased bulk with diminished strength is called pseudohypertrophy, seen in the Duchenne form of muscular dystrophy. Corticospinal tract injury can cause mild atrophy due to decreased muscle use. -When inspecting for atrophy, pay particular attention to the hands, shoulders, thighs, and legs. The spaces between the metacarpals, where the dorsal interosseous muscles lie, should be full or only slightly depressed and hypothenar eminences of the hands should be full and convex. Atrophy of the hand muscles occurs in normal aging ******Furrowing between the metacarpals, and flattening of the thenar and hypothenar eminences (also seen in median and ulnar nerve damage respectively), suggest atrophy. ******Other causes of muscular atrophy include motor neuron diseases, diseases affecting the peripheral motor system projecting from the spinal cord, and protein-calorie malnutrition. *Inspect for fasciculations in atrophic muscles. If absent, tap on the muscles with a reflex hammer, which stimulates them. ******Fasciculations with atrophy and muscle weakness suggest peripheral motor neuron disease.

When upper motor neurons are damaged/when there is a lesion

-functions are reduced or ganglia lost below the level of injury. -When upper motor neuron systems are damaged above their crossover in the medulla, motor impairment develops on the opposite or contralateral side. In damage below the crossover, motor impairment occurs on the same or ipsilateral side of the body. -affected limb becomes weak or paralyzed, and skilled, complicated, or delicate movements are performed poorly when compared with gross movements. -In upper motor neuron lesions, muscle tone is increased and deep tendon reflexes are exaggerated.

posterior columns

-have larger neurons with heavily myelinated axons. -the peripheral large-fiber projections of the dorsal root ganglia transmit the sensations of vibration, proprioception, kinesthesia, pressure, and fine touch from skin and joint position receptors to the dorsal root ganglia where they travel through central projections in the posterior columns to second-order sensory neurons in the medulla. -Fibers projecting from the secondary neurons cross to the opposite side at the medullary level and continue on to the thalamus. ****Diabetic patients with small-fiber neuropathy report sharp, burning, or shooting foot pain, whereas those with large-fiber neuropathy experience numbness and tingling or even no sensation at all.

Weakness

-important to clarify what the patient means—fatigue, apathy, drowsiness, or actual loss of strength. True motor weakness can arise from the CNS, a peripheral nerve, the neuromuscular junction, or a muscle. -Time course and location are especially relevant. Is the onset sudden, gradual or subacute, or chronic, over a long period of time? *****Abrupt onset of motor and sensory deficits occurs in TIA and stroke. Progressive subacute onset of lower extremity weakness suggests Guillain-Barré syndrome. Chronic, more gradual, onset of lower extremity weakness occurs in primary and metastatic spinal cord tumors. -Is the weakness generalized, or focal to the face or a limb? Does it involve one side of the body or both sides? What movements are affected? ****Focal or asymmetric weakness has both central (ischemic, thrombotic, or mass lesions) and peripheral causes ranging from nerve injury to the neuromuscular junction disorders to myopathies. *****Proximal limb weakness, when sym- metric with intact sensation, occurs in myopathies from alcohol, drugs like glucocorticoids, and inflammatory muscle disorders like polymyositis and dermatomyositis. In the neuromuscular junction disorder myasthenia gravis, there is proximal typically asymmetric weakness that gets worse with effort (fatigability), often with associated bulbar symptoms such as diplopia, ptosis, dysarthria, and dysphagia. -To identify proximal weakness, ask about difficulty with movements such as combing hair, reaching up to a shelf, getting up out of a chair, or climbing stairs. Does the weakness get worse with repetition and improve after rest (suggesting myasthenia gravis)? Are there associated sensory or other symptoms? To identify distal weakness, ask about hand strength when opening a jar or using scissors or a screwdriver, or problems tripping when walking. *****Bilateral predominantly distal weak- ness, often with sensory loss, suggests a polyneuropathy, as in diabetes.

The Peripheral Nerves.

-includes spinal and peripheral nerves that carry impulses to and from the cord. A total of 31 pairs of spinal nerves attach to the spinal cord: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. -Each nerve has an anterior (ventral) root containing motor fibers, and a posterior (dorsal) root containing sensory fibers. The anterior and posterior roots merge to form a short spinal nerve, <5 mm long. Spinal nerve fibers commingle with similar fibers from other levels in plexuses outside the cord, from which peripheral nerves emerge. Most peripheral nerves contain both sensory (afferent) and motor (efferent) fibers. -spinal cord contains both gray matter and white matter. The gray matter consists of aggregations of nerve cell nuclei and dendrites that are surrounded by white tracts of nerve fibers connecting the brain to the PNS. Note the butterfly appearance of the gray matter nuclei and their anterior and posterior horns.

muscle strength of the trunk

-may already have assessed during other segments of the examination, namely: ■ Flexion, extension, and lateral bending of the spine ■ Thoracic expansion and diaphragmatic excursion during respiration.

Muscle Tone.

-normal muscle with an intact nerve supply is relaxed voluntarily, it maintains a slight residual tension known as muscle tone -This is best assessed by feeling the muscle's resistance to passive stretch. -Persuade the patient to relax. Hold one hand with yours and, while supporting the elbow, flex and extend the patient's fingers, wrist, and elbow, and put the shoulder through a moderate range of motion. On each side, note muscle tone—the resistance offered to your movements. Tense patients may show increased resistance. ******Decreased resistance suggests dis- ease of the PNS or cerebellum, or the acute stages of spinal cord injury. -If you suspect decreased resistance, hold the forearm and shake the hand loosely back and forth. Normally the hand moves back and forth freely but is not completely floppy. *****Marked floppiness indicates muscle hypotonia or flaccidity, usually from a peripheral motor system disorder. -If resistance is increased, determine if it varies as you move the limb or persists throughout the range of movement and in both directions, for example, during both flexion and extension. Feel for any jerkiness in the resistance. ******Spasticity is velocity-dependent increased tone that worsens at the extremes of range. Spasticity, seen in central corticospinal tract diseases, is rate-dependent, increasing with rapid movement. Rigidity is increased resistance throughout the range of movement and in both directions; it is not rate-dependent. -To assess muscle tone in the legs, support the patient's thigh with one hand, grasp the foot with the other, and flex and extend the patient's knee and ankle on each side. Note the resistance to moving the limb.

Sensory impulses

-participate not only in reflex activity, as previously described, but also give rise to conscious sensation, locate body position in space, and help regulate internal autonomic functions such as blood pressure, heart rate, and respiration.

Herpes Zoster Vaccination.

-results from reactivation of latent varicella (chicken pox) virus infection within the sensory ganglia, usually causes painful unilateral vesicular rashes in a dermatomal distribution. -The herpes zoster vaccine effectively reduces the short-term risks for zoster and postherpetic neuralgia in adults ≥50 years. -Immunization Practices (ACIP) currently recommends routinely offering one- time vaccination for adults ≥60 years

evaluating the sensory system

-test several kinds of sensation: *Pain and temperature (spinothalamic tracts) *Position and vibration (posterior columns) *Light touch (both of these pathways) *Discriminative sensations, which depend on some of the above sensations but also involve the cortex -Assess the patient carefully as you consider the following questions: Is the underlying lesion central or peripheral? Is the sensory loss bilateral or unilateral? Does the pattern of sensory loss suggest a dermatomal distribution, a polyneuropathy, or a spinal cord syndrome with a loss of pain and temperature sensation but intact touch and vibration below a given spinal level? -Because sensory testing is tiring for many patients and can produce unreliable results, conduct the examination as efficiently as possible. Focus on areas that have numbness or pain, motor or reflex abnormalities suggesting a lesion of the spinal cord or PNS, and trophic changes such as absent or excessive sweating, atrophic skin, or cutaneous ulceration. You will often need to retest at another time to confirm abnormalities.

Headache

-warrant thorough assessment -Neurologic causes such as subarachnoid hemorrhage, meningitis, or mass lesions are especially ominous -Always assess the severity of the headache and its location, duration, and any associated symptoms such as double vision, visual changes, weakness, or loss of sensation. -Does the headache get worse with coughing, sneezing, or sudden head movements, which can alter intracranial pressure dynamics? Is there fever, stiff neck, or a parameningeal focus like ear, sinus, or throat infection that may signal meningitis? -Atypical presentation of the patient's usual migraine may be suspicious for stroke, especially in women using hormonal contraceptives -Examine for papilledema and focal neurologic signs ****Primary headaches include migraine, tension, cluster, and trigeminal autonomic cephalagias; secondary headaches arise from underlying structural, systemic, or infectious causes and may be life threatening. ****Subarachnoid hemorrhage classically presents as "the worst headache of my life" with instantaneous onset. Severe headache and stiff neck accompany meningitis. Dull headache increased by coughing and sneezing, especially when recurring in the same location, occurs in mass lesions from brain tumors or abscess. *****Migraine headache is often preceded by an aura or prodrome, and is highly likely if three of the five "POUND" features are present: Pulsatile or throbbing; One- day duration, or lasts 4 to 72 hours if untreated; Unilateral; Nausea or vomit- ing; Disabling or intensity causing inter- ruption of daily activity.

Scale for Grading Reflexes

4- Very brisk, hyperactive, with clonus (rhythmic oscillations between flexion and extension) 3- Brisker than average; possibly but not necessarily indicative of disease 2- Average; normal1 Somewhat diminished; low normal 0- Reflex absent ******Hyperactive reflexes (hyperreflexia) are seen in CNS lesions of the descending corticospinal tract. Look for associated upper motor neuron findings of weakness, spasticity, or a positive Babinski sign. ******Hypoactive or absent reflexes (hyporeflexia) occur in lesions of the spinal nerve roots, spinal nerves, plexuses, or peripheral nerves. Look for associated findings of lower motor unit dis- ease, namely weakness, atrophy, and fasciculations.

Cranial Nerve VII

Facial: -Inspect the face both at rest and during conversation with the patient. Note any asymmetry, often visible in the nasolabial folds, and observe any tics or other abnormal movements. ******Flattening of the nasolabial fold and drooping of the lower eyelid suggest facial weakness. *Ask the patient to: -Raise both eyebrows. -Frown. -Close both eyes tightly so that you can- not open them. Test muscular strength by trying to open them. -Show both upper and lower teeth. -Smile. -Puff out both cheeks. ******A peripheral injury to CN VII, as seen in Bell palsy, affects both the upper and lower face; a central lesion affects mainly the lower face. Loss of taste, hyperacusis, and increased or decreased tearing also occur in Bell palsy *****In unilateral facial paralysis, the mouth droops on the paralyzed side when the patient smiles or grimaces.

The cranial nerves

I. Olfactory nerve: Sense of smell II. Optic nerve: Vision III. Oculomotor nerve: Pupillary constriction, opening the eye (lid elevation), and most extraocular movements IV. Trochlear nerve: Downward, internal rotation of the eye V. Trigeminal nerve: Motor—temporal and masseter muscles (jaw clenching), lateral pterygoids (lateral jaw movement). Sensory—facial. The nerve has three divisions: (1) ophthalmic, (2) maxillary, and (3) mandibular VI. Abducens nerve: Lateral deviation of the eye VII. Facial nerve: Motor—facial movements, including those of facial expression, closing the eye, and closing the mouth Sensory—taste for salty, sweet, sour, and bitter substances on the anterior two thirds of the tongue and sensation from the ear VIII. Vestibulocochlear nerve: Hearing (cochlear division) and balance—(vestibular division) IX. Glossopharyngeal: Motor—pharynxSensory—posterior portions of the eardrum and ear canal, the pharynx, and the posterior tongue, including taste (salty, sweet, sour, bitter) X. Vagus: Motor—palate, pharynx, and larynxSensory—pharynx and larynx XI. Spinal Accessory: Motor—the sternocleidomastoid and upper portion of the trapezius XII. Hypoglossal: Motor—tongue

Stance.

The Romberg Test. -This is mainly a test of position sense. The patient should first stand with feet together and eyes open and then close both eyes for 30 to 60 seconds without support. Note the patient's ability to maintain an upright posture. Normally any swaying is minimal. *****In ataxia from dorsal column disease and loss of position sense, vision compensates for the sensory loss. The patient stands fairly well with eyes open but loses balance when they are closed, a positive Romberg sign. In cerebellar ataxia, the patient has difficulty standing with feet together whether the eyes are open or closed. Test for pronator drift -The patient should stand for 20 to 30 seconds with eyes closed and both arms held straight forward with palms up. Normally patients hold this arm position well. If necessary, patients can be tested in the sitting position. ******Pronator drift occurs when one forearm and palm turn inward and down and is both sensitive and specific for a corticospinal tract lesion in the contralateral hemisphere. Downward drift of the arm with flexion of fingers and elbow is also seen. *Next, instruct the patient to keep the arms out and eyes shut and tap the arms briskly downward. The arms normally return smoothly to the horizontal position. This response requires muscular strength, coordination, and good position sense. *******In loss of position sense the arms drift sideward or upward, sometimes with writhing movements of the hands; the patient may not recognize the dis- placement and when asked, corrects it poorly. In cerebellar incoordination, the arm returns to its original position but overshoots and bounces.

weak- ness of foot dorsiflexion

can be caused by disease of the brain, brainstem, spinal cord, spinal nerve root, peripheral nerve, and muscles.

upper corticospinal tract lesions.

increased function such as heightened muscle tone or pathologic hyperreflexia

Coordination exam

requires four areas of the nervous system to function in an integrated way: ■ The motor system, for muscle strength ■The cerebellar system (also part of the motor system), for normal rhythmic movement and steady posture ■The vestibular system, for balance and for coordinating eye, head,and body movements ■The sensory system, for position sense -To assess coordination, observe the patient performing: ■ Rapid alternating movements ■ Point-to-point movements ■ Gait and other related body movements ■ Standing in specified ways ******In cerebellar disease, look for nystagmus, dysarthria, hypotonia, and ataxia.

Examples for when a neuro exam may seem normal, but there is an underlying issue

when a patient recovers from attacks of epilepsy or a transient ischemic attack (TIA). In some neurologic diseases such as migraine, normal findings are expected—abnormal findings would trigger alarm and further evaluation. In some instances, symptoms in the absence of findings would raise concern, as with a TIA

Tips for Detecting Sensory Deficits

● Compare symmetric areas on the two sides of the body, including the arms, legs, and trunk. -A hemisensory loss pattern suggests a lesion in the contralateral cerebral hemisphere; a sensory level (when one or more sensory modalities are reduced below a dermatome on one or both sides) suggests a spinal cord lesion. -For pain, temperature, and touch sensation, compare distal to proximal areas of the extremities. Scatter the stimuli to sample most of the dermatomes and major peripheral nerves. One suggested pattern is to include: ● both shoulders (C4) ● the inner and outer aspects of the forearms (C6 and T1) ● the thumbs and little fingers (C6 and C8) ● the fronts of both thighs (L2) ● the medial and lateral aspects of both legs (L4 and L5) ● the little toes (S1) ● the medial aspect of each buttock (S3) ● For vibration and position sensation, test the fingers and toes first. If these are normal, you may safely assume that more proximal areas are also be normal. ● Vary the pace of your testing so that the patient does not merely respond to your repetitive rhythm. ● When you detect an area of sensory loss or hypersensitivity, map out its boundaries in detail. Stimulate first at a point of reduced sensation, then in progressive steps until the patient reports a change to normal sensation. An example is shown here. ******Symmetric distal sensory loss suggests a diabetic polyneuropathy. You may miss this finding unless you compare distal and proximal sensation. ******Here, all sensation in the hand is lost. Repetitive testing in a proximal direction reveals a gradual return to normal sensation at the wrist. This pattern does not fit either peripheral nerve damage or dermatomal loss. If bilateral, it suggests the "glove" of the "stocking- glove" sensory loss of polyneuropathy, often seen in alcoholism and diabetes. -The patient's eyes should be closed during actual testing.

Guiding Questions for Examination of the Nervous System

● Does the patient have neurologic disease? ● If so, what is the localization of the lesion or lesions? Are your findings symmetric? ● What is the pathophysiology of abnormal findings? ● What is the preliminary differential diagnosis? When you conduct the neurologic examination, it is wise to adopt a fixed rou- tine or examination sequence to minimize omission of one of its important components.

Common or Concerning Symptoms (Nerve exam)

● Headache ● Dizziness or vertigo ● Weakness (generalized, proximal, or distal) ● Numbness, abnormal or absent sensation ● Fainting and blacking out (near-syncope and syncope) ● Seizures ● Tremors or involuntary movements