Neurologic Exam

Question 1

6 main subdivisions of the neurologic exam

Answer 1

1. mental status
2. cranial nerves
3. motor exam
4. reflexes
5. coordination and gait
6. sensory exam

Question 2

Tests for attention

Answer 2

World spelled backward. months backward. digits forward (6) and backward (4 is normal)

Question 3

Anterograde amnesia

Answer 3

difficulty remembering new facts and events

Question 4

Retrograde amnesia

Answer 4

impaired memory of events for a period of time immediately before lesion onset, with relative sparing of earlier memories.

Question 5

Tests of memory

Answer 5

ask to recall 3 items or a brief story 3 to 5 minutes later.

Question 6

Spontaneous speech

Answer 6

note the patient’s fluency, including phrase length, rate, and abundance of spontaneous speech. Note tonal modulation and paraphasic errors (inappropriately substituted words or syllables), neologisms (nonexistent, invented words), or errors in grammar.

Question 7

Comprehension

Answer 7

can the patient understand simple questions and commands? comprehension of grammatical structure should be tested as well: “Mike was shot by John. Is John dead?”

Question 8

Naming

Answer 8

Ask the patient to name easy objects (pen, watch, tie, etc.) and some more difficult to name objects (fingernail, belt buckle, stethoscope, etc). Naming parts of objects is more difficult and should be tested.

Question 9

Repetition

Answer 9

can they repeat single words and sentences (No ifs, ands, or buts)

Question 10

Reading

Answer 10

ask the patient to read aloud single words, a brief passage, and the front page of a newspaper and test for comprehension.

Question 11

Writing

Answer 11

Ask the patient to write their name and write a sentence.

Question 12

Gerstmann’s syndrome

Answer 12

impairment in calculation, right-left confusion, finger agnosia, and agraphia. Caused by lesions in the dominant parietal lobe, thus, aphasia is often (but not always) present as well, which can make the diagnosis difficult or impossible.

individually, these 4 can be seen in many different lesions and may be present in individuals with impaired attention, language, praxis, constructions, logic and abstraction, and so on.

Question 13

Calculations

Answer 13

can the patient do simple addition, subtraction, and so on?

Question 14

Right-left confusion

Answer 14

can the patient identify right and left body parts?

“Touch your right ear with your left thumb.”

Question 15

Finger Agnosia

Answer 15

can the patient name and identify each digit?

“Touch your right ear with your left thumb.”

Question 16

Agraphia

Answer 16

Can the patient write their name and a sentence?

Question 17

Apraxia

Answer 17

inability to follow a motor command, when this inability is not due to a primary motor deficit or a language impairment. Caused by a deficit in higher-order planning or conceptualization of the motor task.

Pretend to comb your hair

Pretend to strike a match and blow it out

This can be caused by lesions in any of many different regions, so exact localization is often difficult. Apraxia is commonly present in lesions affecting the language areas and adjacent structures of the dominant hemisphere. This can be hard to distinguish (language deficit vs. apraxia). The distinction can often be made by asking patients to perform a task; and then if the patient fails, demonstrate several tasks and ask them to choose the correct one.

Question 18

Neglect and constructions

Answer 18

hemineglect is an abnormality in attention to one side of the universe that is not due to a primary sensory or motor disturbance. In sensory neglect, patients ignore visual, somatosensory, or auditory stimuli on the affected side, despite intact primary sensation. This can often be demonstrated by testing for extinction on double simultaneous stimulation.

Motor neglect: can have normal strength on testing, but may not move the affected limb unless attention is strongly directed toward it.

may see visual neglect on line bisection task or on clock drawing task.

Question 19

Anosognosia

Answer 19

“Is anything wrong with you right now?”

Question 20

Hemineglect

Answer 20

most common in lesions of the right (nondominant) parietal lobe, causing patients to neglect the left side. Left-sided neglect can also occasionally be seen in right frontal lesions, right thalamic or basal ganglia lesions, and rarely, in lesions of the right midbrain. In left parietal lesions a much milder neglect is usually seen, affecting the patient’s right side.

visual hemineglect or extinction is usually caused by contralateral parietal lesions and less often by frontal or thalamic lesions.

Question 21

Sequencing tasks and frontal release signs

Answer 21

patients with frontal lobe dysfunction may have particular difficulty in changing from one action to the next when asked to continue drawing a repeated sequence of actions. They may get stuck on one shape and keep drawing it, demonstrating perseveration. You can also see perseveration on fist, edge, palm.

Motor impersistence: a form of distractibility in which patients only briefly sustain a motor action in response to a command such as “raise your arms” or “look to the right.”

Ability to suppress inappropriate behaviors can be tested by the Auditory Go-No-Go Test, in which the patient moves a finger in response to one tap on the table but must keep it still in response to two taps.

Frontal release signs:
Grasp reflex-

Frontal lesions may also result in abulia or other personality changes and judgment issues reported by family.

Question 22

Logic and Abstraction

Answer 22

Can they solve simple problems such as the following: “If Mary is taller than Jane and Jane is taller than Ann, who’s the tallest?”

How does the patient interpret proverbs, such as “don’t cry over spilled milk?”

How well can they comprehend similarities such as “How are a car and an airplane alike?”

How well can they generalize and complete a series- for example, “Continue the following: AZ, BY, CX, D__”

These functions can be abnormal in damage to a variety of brain areas involving higher-order association cortex and are not well localized.

Question 23

Delusions and Hallucinations

Answer 23

Does the patient have any delusional thought processes? Does the patient have auditory or visual hallucinations?

May also ask, “Do you feel that someone is watching you or trying to hurt you?” or “Do you have any special abilities or powers?”

Can be seen in toxic or metabolic abnormalities and other causes of diffuse brain dysfunction as well as in primary psychiatric disorders. Abnormal sensory phenomena can also be caused by focal lesions or seizures in visual, somatosensory, or auditory cortex, and thought disorders can be caused by lesions in the association cortex and limbic system.

Question 24

Mood

Answer 24

any signs of depression, anxiety, or mania?

usually considered psychiatric in origin and may be due to imbalances in neurotransmitter systems in several different areas of the brain. However, features of these disorders are also seen in focal brain lesions and in toxic and metabolic abnormalities such as thyroid dysfunction.

Question 25

Olfaction (CNI)

Answer 25

Can the patient smell coffee or soap with each nostril?

Impairment can be due to nasal obstruction, damage to the olfactory nerves in the nasal mucosa, damage to the nerves as they cross the cribiform plate, or intracranial lesions affecting the olfactory bulbs.

Question 26

CN II (Optic Nerve)

Answer 26

Examine both retinas carefully with an ophthalmoscope to visualize any damage to the retina or retinal vessels, optic nerve atrophic changes, papilledema, and other important abnormalities.

Vision- test visual acuity for each eye separately (by covering one eye at a time), using an eye chart.

Color vision: test each eye separately for ability to distinguish colors. Test for red desaturation, a sign of subtle asymmetry in optic nerve function (as seen, for example in optic neuritis), by asking the patient to cover each eye alternately while looking at a red object and to report any relative dullness of the color as viewed through either eye.

Visual fields. Test visual fields for each eye by asking the patient to fixate straight ahead and to report when a finger can be seen moving in each quadrant.

Visual extinction. test for visual extinction on double simultaneous stimulation by asking patients how many fingers they see when fingers are presented to both sides at the same time. In visual extinction, a form of hemineglect, patients do not report seeing the fingers on the affected (usually left) side of the visual field, although they can see them when they are presented to one side alone.

Question 27

Pupillary Responses (CN II, III)

Answer 27

record pupil size and shape at rest. then note the direct response, meaning constriction of the illuminated pupil, as well as the consensual response, meaning constriction of the opposite pupil. the direct response is impaired in lesions of the ipsilateral optic nerve, the pretectal area, the ipsilateral parasympathetics traveling in CN III, or the pupillary constrictor muscle of the iris.

In an afferent pupil defect there is a decreased direct response caused by decreased visual function (CN II) in one eye. however, there is spared pupillary constriction (CN III) when elicited through the consensual response. This can be demonstrated with the swinging flashlight test, in which the light is moved back and forth between the eyes every 2 to 3 seconds. The afferent pupillary defect becomes obvious when the flashlight is moved from the normal to the affected eye and the affected pupil dilates instead of constricting in response to light. brief oscillations of pupillary size called hippus occur normally in response to light and should not be confused with an afferent pupillary defect. The consensual response (contralateral pupil illuminated) is impaired in lesions of the contralateral optic nerve, the pretectal area, the ipsilateral parasympathetics traveling in CN III, or the pupillary constrictor muscle.

Finally, test pupillary response to accommodation (also called the near response). Normally, the pupils constrict while fixating on an object being moved toward the eyes. Accommodation (response to looking at something moving toward the eye) is impaired in lesions of the ipsilateral optic nerve, the ipsilateral parasympathetics traveling in CN III, the pupillary constrictor muscle, or in bilateral lesions of the pathways from the optic tracts to the visual cortex. Accommodations to near stimuli is spared in lesions of the pretectal area that may impair the pupillary light response, a condition called “light-near dissociation.”

Question 28

Extraocular movements (CN III, IV, VI)

Answer 28

check by having the patient look in all directions without moving their head. While doing this, ask them if they experience any double vision. Test smooth pursuit by having the patient follow an object moved across their full range of horizontal and vertical eye movements.

Test convergence movements by having the patient fixate on an object as it is moved slowly toward a point right between their eyes.

Observe the eyes at rest to see if there are any abnormalities such as spontaneous nystagmus or dysconjugate gaze (eyes not both fixated on the same point), resulting in diplopia (double vision).

Saccades are eye movements used to rapidly refixate from one object to another. Test saccades by holding up two widely spaced targets (thumb and forefinger on opposite hands) and ask patient to look back and forth between the targets (by saying “now look at my finger, thumb, finger, thummb..”

Test optokinetic nystagmus by moving a strip with parallel stripes on it in front of the patient’s eyes and asking them to watch the stripes go by. Normally, rhythmic eye movements called nystagmus occur, consisting of an alternating slow phase, with slow pursuit movements in the direction of strip movement, and a rapid phase, with quick, saccadic refixations back to midline. OKN testing can be very useful in detecting subtle abnormalities or asymmetries in saccadic or smooth pursuit eye movements.

Spontaneous nystagmus can indicate toxic or metabolic conditions such as drug overdose, alcohol intoxication, or peripheral or central vestibular dysfunction.

Question 29

Facial sensation and muscles of mastication (CN V)

Answer 29

Test facial sensation using a cotton wisp and a sharp object. Also test for tactile extinction, using double simultaneous stimulation. The corneal reflex, which involves both CN V and VII, is tested by touching each cornea gently with qtip and observing any asymmetries in the blink response.

Feel the masseter muscles during jaw clench. Test for a jaw jerk reflex by gently tapping on the jaw with the mouth slightly open.

Facial sensation can be impaired by lesions of the trigeminal nerve (CN V), the trigeminal sensory nuclei in the brainstem, or ascending sensory pathways to the thalamus and somatosensory cortex in the postcentral gyrus. The corneal reflex is mediated by polysynaptic connections in the brainstem between CN V and facial CN II nerves and can be impaired by lesions anywhere in this circuit.

Extinction in the presence of intact primary sensation is usually caused by right parietal lesions.

Presence of jaw jerk reflex is abnormal, especially if prominant. it is a sign of hyperreflexia associated with lesions of upper motor neuron pathways projecting to the trigeminal motor nucleus. Mediated by CN V.

Question 30

Muscles of facial expression and taste (CN VII)

Answer 30

look for asymmetry in facial shape or in depth of furrows such as the nasolabial fold. look for asymmetries in spontaneous facial expressions and blinking. facial weakness may be difficult to detect in cases where it occurs bilaterally, also known as facial diplegia, because the facial weakness is symmetrical.

Ask patients to smile, puff out cheeks, clench eyes tight, wrinkle their brow, and so on. can use old photos of the patient to aid in recognition of subtle changes.

Check taste with sugar, salt, or lemon juice on cotton swabs applied to the lateral aspect of each side of the tongue. Like olfaction, taste is often tested only when specific pathology is suspected, such as in lesions of the facial nerve or in lesions of the gustatory nucleus.

Facial weakness can be due to lesions of UMN in the contralateral motor cortex or descending CNS pathways, LMN in the ipsilateral face nerve nucleus or exiting fibers, the neuromuscular junction, or the face muscles. Note that the UMN for the upper face (the upper portions of the orbicularis oculi and the frontalis muscles of the forehead) project to the facial nuclei bilaterally. Therefore, UMN lesions such as in stroke cause contralateral face weakness, sparing the forehead, while LMN lesions such as in facial nerve injury typically cause weakness involving the whole ipsilateral face.

unilateral deficits in taste can occur in lesions of the lateral medulla involving the nucleus solitarius or in lesions of the facial nerve.

Question 31

Hearing and vestibular sense (CN VIII)

Answer 31

can the patient hear fingers rubbed together or words whispered just outside of the auditory canal and identify which ear hears the sound? A tuning fork can be used to distinguish neural from mechanical conductive hearing problems. Vestibular sense is generally not specifically tested except in the following important situations:

1. Vertigo: Certain maneuvers can help distinguish central from peripheral lesions
2. patients with limitations of horizontal or vertical gaze. testing vestibulo-ocular reflex can help localize the lesion. the vestibuloocular reflex can be tested either using the oculocephalic maneuver, in which the eyes are held open and the head is turned rapidly either from side to side or up and down, or by using caloric testing, in which cold or warm water is instilled into one ear, producing asymmetrical stimulation of the semicircular canals.
3. Patients in coma: The vestibulo-ocular reflex is often the only way to test eye movements in these patients.

hearing loss can result from lesions in the acoustic and mechanical elements of the ear, the neural elements of the cochlea, or the acoustic nerve (VIII). After the hearing pathways enter the brainstem, they cross over at multiple levels and ascend bilaterally to the thalamus and auditory cortex. Thus, clinically significant unilateral hearing loss is invariably caused by peripheral neural or mechanical issues.

Question 32

Palate elevation and gag reflex (CN IX, X)

Answer 32

Does the palate elevate symmetrically when the pateint says, “Aah”? Does the patient gag when the posterior pharynx is brushed? The gag reflex needs to be tested only in patients with suspected brainstem pathology, impaired consciousness, or impaired swallowing.

Palate elevation and gag reflex are impaired in lesions involving the CN IX and X, the neuromuscular junction, or the pharyngeal muscles.

Question 33

Muscles of articulation (CN V, VII, IX, X, XII)

Answer 33

is the patient’s speech hoarse, slurred, quiet, breathy, nasal, low or high pitched, or otherwise unusual? ask if patient’s speech has changed from baseline. Dysarthria is abnormal pronunciation of speech (slurred speech), and should be distinguished from aphasia, which is an abnormality in language production or comprehension.

Abnormal articulation of speech can occur in lesions involving the muscles of articulation, the neuromuscular junction, or the peripheral or central portions of CN V, VII, IX, X, or XII. Speech can also be abnormal as a result of lesions in the motor cortex, cerebellum, basal ganglia, or descending pathways to the brainstem.

Question 34

Sternocleidomastoid and trapezius muscles (CN XI)

Answer 34

ask the patient to shrug their shoulders, turn their head in both directions, and raise their head from the bed, flexing forward against the force of your hands.

weakness in the sternocleidomastoid or trapezius muscles can be caused by lesions in the muscles, neuromuscular junction, or lower motor neurons of the accessory spinal nerve (CN XI). Unilateral UMN lesions in the cortex or descending pathways cause contralateral weakness of the trapezius, with relative sparing of sternocleidomastoid strength. This may be remembered by analogy to UMN facial lesions sparing the upper portion of the face. When sternocleidomastoid weakness is present with UMN lesions, there is weakness of head turning away from the side of the lesion.

Question 35

Tongue Muscles (CN XII)

Answer 35

Note any atrophy or fasciculations (spontaneous, quivering movements) of the tongue while it is resting on the floor of the mouth. Ask the patient to stick their tongue straight out and note whether it curves to one side or the other. Ask them to move their tongue from side-to-side and to push it forcefully against the inside of their cheek.

fasciculations and atrophy are signs of lower motor neuron lesions. Unilateral tongue weakness causes the tongue to deviate toward the weak side. Tongue weakness can result from lesions of the tongue muscles, the neruomuscular junction, the LMN of the hypoglossal nerve, or the UMNs originating in the motor cortex. Lesions of the motor cortex cause contralateral tongue weakness.

Question 36

Motor Exam steps

Answer 36

1. observation
2. inspection
3. palpation
4. muscle tone testing
5. functional testing
6. strength testing of individual muscle groups

Question 37

Motor exam: Observation

Answer 37

observe patient to detect twitches, tremors, or other involuntary movements, as well as any unusual paucity of movement. Note their posture.

involuntary movements and tremors are commonly associated with lesions of the basal ganglia or cerebellum. Tremors can occasionally be seen with peripheral nerve lesions.

Question 38

Signs of UMN and LMN lesions

Answer 38

UMN vs. LMN
Weakness: Yes, Yes
Atrophy: No, Yes
Fasciculations: No, Yes
Reflexes: Increased, Decreased
Tone: Increased, Decreased

many parts of the motor exam can help distinguish between UMN and LMN lesions. Recall that UMNs project via the corticospinal tract to LMNs located in the anterior horn of the spinal cord. Signs of LMN lesions include weakness, atrophy, fasciculations, and hyporeflexia (reduced reflexes). Signs of UMN lesions include weakness, hyperreflexia (increased reflexes), and increased tone. The hyperreflexia and increased tone seen with corticospinal lesions is apparently caused by damage to pathways that travel in close association with the corticospinal tract rather than directly by damage to the tract itself. Note that with acute UMN lesions there is often flaccid paralysis, with decreased tone and decreased reflexes. With time (hours to weeks), increased tone and hyperreflexia usually develop.

Question 39

Motor Exam: Inspection

Answer 39

inspect several individual muscles to see if muscle wasting, hypertrophy, or fasciculations are present. the best muscle to look at for fasciculations in generalized LMN disorders are the intrinsic hand muscles, shoulder girdle, and thigh

Question 40

Motor Exam: Palpation

Answer 40

in cases of suspected myositis, palpate the muscles to see if there is tenderness

Question 41

Motor Exam: Muscle tone testing

Answer 41

ask the patient to relax, and then passively move each limb at several joints to get a feeling for any resistance or rigidity that may be present.

many parts of the motor exam can help distinguish between UMN and LMN lesions. Recall that UMNs project via the corticospinal tract to LMNs located in the anterior horn of the spinal cord. Signs of LMN lesions include weakness, atrophy, fasciculations, and hyporeflexia (reduced reflexes). Signs of UMN lesions include weakness, hyperreflexia (increased reflexes), and increased tone. The hyperreflexia and increased tone seen with corticospinal lesions is apparently caused by damage to pathways that travel in close association with the corticospinal tract rather than directly by damage to the tract itself. Note that with acute UMN lesions there is often flaccid paralysis, with decreased tone and decreased reflexes. With time (hours to weeks), increased tone and hyperreflexia usually develop.

Increase tone can occur in UMN lesions but can also occur in basal ganglia dysfunction. In addition, slow or awkward fine finger movements or toe tapping in the absence of weakness can signify a subtle abnormality of the corticospinal pathways, but these findings can also occur in lesions of the cerebellum or basal ganglia.

Question 42

Motor Exam: Functional testing

Answer 42

helps detect subtle abnormalities. check for drift by having the patient hold up both arms simultaneously or both legs simultaneously with eyes closed. check fine movements by testing rapid finger tapping, rapid hand pronation-supination (as in screwing in a light bulb), rapid hand tapping, and rapid foot tapping against the floor or other object.

Question 43

Muscle strength rating scale

Answer 43

0/5: No contraction

1/5: Muscle flicker, but no movement

2/5: Movement possible, but not against gravity (test the joint in its horizontal plane)

3/5: Movement possible against gravity, but not against resistance by the examiner

4: Movement possible against some resistance by the examiner (sometimes this category is subdivided further into 4-/5, 4/5, 4+/5)
5: Normal strength

Question 44

Deep Tendon Reflexes

Answer 44

check using impulses from a reflex hammer to stretch the muscle and tendon. the limbs should be in a relaxed and symmetrical position, since these factors can influence reflex amplitude.

Clonus is sometimes seen when reflexes are very brisk. this is a sign of hyperreflexia, as is spreading of reflexes to other muscles not directly being testedand crossed adduction of the opposite leg when the medial aspect of the knee is tapped. hoffman’s sign indicates heightened reflexes involving the finger flexor muscles.

Rating scale:
0: absent reflex

1+: Trace, or seen only with reinforcement

2+: Normal

3+: Brisk

4+: Nonsustained clonus (i.e., repetitive vibratory movements)

5+: Sustained clonus

1,2,3 are normal unless asymmetrical. 0, 4,5 are abnormal

deep tendon reflexes may be diminished by abnormalities in muscles, sensory neurons, lower motor neurons, and the neuromuscular junction; acute upper motor neuron lesions; and mechanical factors such as joint disease. Abnormally increased reflexes are associated with UMN lesions. Note that deep tendon reflexes can be influenced by age, metabolic factors such as thyroid dysfunction or electrolyte abnormalities, and the anxiety level of the patient.

Question 45

Clonus

Answer 45

a repetitive vibratory contraction of the muscle that occurs in response to muscle and tendon stretch.

Question 46

Plantar response

Answer 46

scrape an object across the sole of the foot beginning from the heel, moving forward toward the small toe, and then arcing medially toward the big toe. Normal response is downward contraction of the toes.

Abnormal response is Babinski’s sign, characterized by an upgoing big toe and fanning outward of the other toes. If toes are silent on one side (no movement either way) but normal on the other, this is abnormal. Babinski is normal until about 1 year old then abnormal. It is associated with UMN lesion anywhere along the corticospinal tract.

Question 47

Frontal Release Signs

Answer 47

Frontal lobe lesions in adults can cause re-emergence of certain primitive reflexes that are normally present in infants but are pathological in adults.

includes grasp, snout, root, and suck reflexes.

Question 48

Glabellar response and palmomental reflex

Answer 48

glabeller response: Tap with a finger repeatedly in the midline between the eyes and ask the patient to keep their eyes open. the normal patient may blink a few times, but the response extinguishes. the abnormal response- continued blinking with each tap (Myerson’s sign) - is most commonly seen in neurodegenerative movement disorders such as Parkinson’s disease.

Palmomental reflex: scraping the hypothenar eminence causes ipsilateral contraction of the mentalis muscles of the chin. This response is very non-specific, and is present in some normal individuals.

Question 49

Posturing

Answer 49

can be seen with damage to descending motor pathways. consists of complex reflexes involving brainstem and spinal cord circuitry.

special reflexes tested in spinal cord lesions help localize the level of damage. frontal release signs support the localization of lesions to the frontal lobes.

Question 50

Coordination

Answer 50

usually described under a separate section from motor exam b/c cerebellar disorders can disrupt coordination and gait while leaving other motor functions intact. disturbance of coordination and gait can be caused by lesions in many systems other than the cerebellum.

see: ataxia, dysdiadochokinesia- as features of coordination disorders

Popular test of coordination is finger-nose-finger test- patient is asked to alternately touch their nose and the examiner’s finger as quickly as possible. Hold examiner’s finger at extreme of patient’s reach and can also occasionally move suddenly to different location. test for overshoot by having patient raise both arms suddenly from their lap to the level of your hand.

heel-shin test: patient is asked to touch the heel of one foot to the opposite knee and then to drag their heel in a straight line all the way down the front of their shin and back up again. in order to eliminate the effect of gravity in moving the heel down the shin, this test should always be done in the supine position.

Normal performance of these motor tasks depends on the integrated functioning of multiple sensory and motor subsystems. these include position sense pathways, visual pathways, lower motor neurons, upper motor neurons, the basal ganglia, and the cerebellum. Thus, in order to convincingly demonstrate that abnormalities are due to a cerebellar lesion, one must first test for normal joint position sense, vision, strength, and reflexes and confirm the absence of involuntary movements caused by basal ganglia lesions.

Question 51

Ataxia

Answer 51

describes the abnormal movements seen in coordination disorders. In ataxia there are medium-to-large-amplitude involuntary movements with an irregular oscillatory quality superimposed on and interfering with the normal smooth trajectory of movement. Overshoot is also commonly seen as a part of ataxic movements and is sometimes referred to as past pointing when target-oriented movements are being discussed.

Appendicular ataxia: affects movements of the extremities and is usually caused by lesions of the cerebellar hemispheres and associated pathways.

Truncal ataxia affects the proximal musculature, especially that is involved in gait stability, and is caused by midline damage to the cerebellar vermis and associated pathways.

Question 52

Dysdiadochokinesia

Answer 52

abnormal alternating movements. another feature of coordination disorders.

Question 53

Romberg Test

Answer 53

ask patient to stand with feet together. then ask the patient to close eyes. Remain close at hand in case the patient begins to sway or fall.

with the eyes open, 3 sensory systems provide input to the cerebellum to maintain truncal stability. these are vision, proprioception, and vestibular sense. If there is a mild lesion in the vestibular or proprioception systems, when the eyes are open the patient is usually able to compensate and remain stable. When the patient closes their eyes, visual input is removed and instability can be brought out. in more severe lesions or midline cerebellar lesions, the patient will be unable to maintain this position even with their eyes open.

Question 54

Gait

Answer 54

observe walking toward you and away from you in an open area with plenty of room. Note stance (how far apart the feet are), posture, stability, how high the feet are raised off the floor, trajectory of leg swing and whether there is circumduction (an abnormal arced trajectory in the medial to lateral direction), leg stiffness and degree of knee bending, arm swing, tendency to fall or swerve in any particular direction, rate and speed, difficulty initiating or stopping gait, and any involuntary movements that are brought out by walking. Turns should also be observed closely.

to bring out abnormalities in gait and balance, you can do tandem gait (ask patient to walk a straight line while touching the heel of one foot to the toe of the other). those with truncal ataxia have particular difficulty with this as they tend to have wide based, unsteady gait.

Gait apraxia: (somewhat controversial) abnormality in which patient is able to carry out all of the movements required for gait normally when lying down but is unable to walk in the standing position. thought to be associated with frontal disorders and NPH

Gait involves multiple sensory and motor systems. Vision, proprioception, vestibular sense, LMN, UMN, basal ganglia, cerebellum, and higher-order motor planning systems in the association cortex. again, must test all for normal function before concluding that a gait disturbance is caused by cerebellum.

Question 55

Primary sensation

Answer 55

pain sensation with sharp or dull end of a safety pin. light touch with a qtip. temperature sense wtih a cool piece of metal such as a tuning fork. Vibration sense by placing a vibrating tuning fork on the ball of the patietns right or left large toe or fingers and asking them to report when the vibration stops. (low freq. 128 or even 64 Hz). dont place tuning fork on bone. Test joint position sense by moving one finger or toe upward and downward and asking to report which way it moves.

Question 56

Cortical sensation

Answer 56

graphesthesia: patients close eyes and identify letters or numbers that are being traced onto their palm or finger tip.

Stereognosis: patients close eyes and identify various objects by touch, using one hand at a time.

Tactile extinction.

these cannot reliably be tested for unless primary sensation is intact bilaterally.

Somatosensory deficits can be caused by lesions in peripheral nerves, nerve roots, the posterior columns or anterlateral sensory systems in the spinal cord or brainstem, thalamus, or sensory cortex. Position and vibration sense ascend in the posterior column pathway and cross over in the medulla, while pain and temp sense cross over shortly after entering the spinal cord and then ascend in the anterolateral pathway. intact primary sensation with deficits in cortical sensation such as agraphesthesia or astereognosia suggests a lesion in the contralateral sensory cortex. however, severe cortical lesions can cause deficits in primary sensation as well.

extinction with intact primary sensation is a form of hemineglect usually associated with lesions of right parietal lobe. can also be seen occasionally in right frontal or subcortical lesions, or in left hemisphere lesions causing mild right hemineglect.

Question 57

Posturing reflexes

Answer 57

seens in patietns with damage to the descending UMN pathways. These reflexes depend on brainstem and spinal circuitry and are often seen in severe lesions associated with coma.

Decorticate posturing: flexor posturing, where upper limbs flex to painful stimuli. tend to occur wtih lesions higher in the neuroaxis, at the midbrain or above

Decerebrate posturing: extensor posturing- both upper and lower limbs extend. tends to occur with more severe lesions extending lower down in the brainstem.