Neuro Exam Flashcards Preview

NEUROLOGY 🧠 > Neuro Exam > Flashcards

Flashcards in Neuro Exam Deck (22)
Loading flashcards...
1
Q

Alertness

A

The patient must be awake and alert in order to have a “window” to view the cortex. So assessment of the level of alertness and the intactness of the reticular activating system is the first step in the mental status assessment.

2
Q

Orientation:

A

MMSE:

Time (year, season, month, date, and day of the week) 5

Place (state, county, city, building, and floor or room) 5

3
Q

Memory

A

MMSE:

Registration: Repeat names of three objects (1 point per object) 3

Attention and Calculation: Spelling world backwards; Serial 7’s 5

Recent memory: Three-word recall 3

Remote memory tasks such as naming Presidents, tests not only the temporal lobes but also heteromodal association cortices.

Attention-working memory: Digit span (529682), and naming months of the year backward test attention and working memory which are frontal lobe functions, set generation such as naming lists of things in a certain category.

Judgement-abstract reasoning - neighbors house on fire; alike apple fruits; happy sad, doctor nurse; proverbs

Set generation: This is a test of verbal fluency and the ability to generate a set of items which are frontal lobe functions. Most individuals can give 10 or more words in a minute.

4
Q

Language: Temporal and Frontal Lobes

A

Language: Name a pencil and watch 2

Repeat “No If’s ands or buts” 1

Receptive language: Wernicke’s area, which is located in the posterior part of the superior temporal gyrus of the dominant temporal lobe. Asking the patient to follow commands demonstrates that they understand the meaning of what they have heard or read. It is important to test reception of both spoken and written language.

Follow three step command “Take this and place it in my right hands, point to the ceiling after you point to the floor, fist-edge-palm” 3

Expressive language: Broca’s area located in posterior part of the inferior frontal gyrus of the dominant hemisphere. Homologous regions of the non-dominant hemisphere are important for the non-verbal contextual and emotional aspects as well as the prosody (rhythm) of language. Tests for written and spoken receptive and expressive language are used to “view” these language centers. In assessing expressive language it is important to note fluency and correctness of content and grammar. This can be accomplished by tasks that require spontaneous speech and writing, naming objects, repetition of sentences, and reading comprehension.

Read and follow “close your eyes” 1

write a complete sentence” 1

Copy** two intersecting pentagons **1

Frontal release signs:

The snout reflex is elicited by gently tapping the lips and results in their protrusion.

The glabellar reflex is elicited by repetitive tapping on the forehead just above the nose; normal subjects blink only in response to the first several taps, whereas persistent blinking is an abnormal response (Myerson sign).

5
Q

Parietal lobes: Important for perception and interpretation of sensory information especially somatosensory information. The non-dominant parietal lobe is particularly important for visual-spatial function. The dominant parietal lobe is important for praxis, which is the formation of the idea of a complex purposeful motor act while the frontal lobes are important for the execution of the act.

Gerstmann syndrome: Constellation of acalculia, finger agnosia, right-left confusion and agraphia, occurs with damage to the dominant inferior parietal lobe. MCA on dominant inf. parietal lobe.

Agnosia inability to identify objects by tactile exploration. Asterognosis is tactile agnosia when only 1 limb is affected.

Praxis The patient is asked to perform skilled motor tasks without any nonverbal prompting. Skills tested for should involve the face then the limbs. In order to test for praxis the patient must have normal comprehension and intact voluntary movement. Apraxia is typically seen in lesions of the dominant inferior parietal lobe.

“Pretend you are sucking on a straw; blowing a kiss; opening a door; R thumb on L elbow” ‘How would you cut a paper with scissors”

Apraxia (inability to perform purposeful motor acts on command)

Constructional apraxia (inability to draw objects which require use of visual spatial organization)

Gnosis is the ability to recognize objects perceived by the senses especially somatosensory sensation. Having the patient (with their eyes closed) identify objects placed in their hand (stereognosis) and numbers written on their hand (graphesthesia) tests parietal lobe sensory perception

Dominant parietal lobe function: Right-left orientation, naming fingers, and calculations.

“Which is my right hand”; 100 -7

Non dominant parietal lobe Important for visual spatial sensory tasks such as attending to the contralateral side of the body and space as well as constructional tasks such as drawing a face, clock or geometric figures.

Clock Drawing (=“Mini-cog”, dementia, executive dysfunction, construction apraxia), Word association, trailmaking

A
6
Q

Visual recognition: Occipital lobes

Recognition of colors and faces tests visual association cortex (inferior occiptotemporal area)[fusiform gyrus]. Achromatopsia (inability to distinguish colors), visual agnosia (inability to name or point to a color) and prosopagnosia (inability to identify a familiar faces) result from lesions in this area.

“Naming of objects, naming of colors and recognition of faces”.

A
7
Q

Cranial Nerve Examination

A

Inspection orbital area, conjunctiva, sclera, iris,

Examination of the cranial nerves allows one to “view” the brainstem all the way from its rostral to caudal extent. The cranial nerves for each of these are: 2 for the midbrain (CN 3 & 4), 4 for the pons (CN 5-8), and 4 for the medulla (CN 9-12). It is important to remember that cranial nerves never cross (except for one exception, the 4th CN) and clinical findings are always on the same side as the cranial nerve involved.

The cranial nerves are part of the PNS with the exception of the optic nerve (cranial nerve II), along with the retina.

8
Q

CN1

A

Olfaction is the only sensory modality with direct access to cerebral cortex without going through the thalamus. Loss of smell is anosmia. The most common cause is a cold or nasal allergies. Other causes include trauma or a meningioma affecting the olfactory tracts. Anosmia is also seen in Kallman syndrome because of agenesis of the olfactory bulbs.

9
Q

CN2

A

Visual acuity can be done with a standard Snellen chart or with a pocket chart (Rosenbaum). Have the patient use their glasses if needed to obtain best-corrected vision.

Visual fields (“is my face symmetric; do my hands look the same x3) Test each eye individually using your fingers in the four quadrants of the visual field and ask the patient to count fingers held up or point to the hand when a finger wiggles using yourself as a control. A second screening test is to use a grid card. Have the patient focus on the dot in the center of the grid then ask if any part of the grid is missing or looks different.

Ophthalmoscopy: Direct visualization of the optic nerve head is an important and valuable part of assessing CN 2. Systematically look at the optic disc, vessels, retinal background and fovea:

Optic Disk: The optic disk is usually easily recognizable as a yellowish, slightly oval structure situated nasally at the posterior pole of the eye. The disk margins should be sharply demarcated. Blood vessels crossing the border of the optic disk are distinct, pulsatile, and become obscured when the disk swells.

Optic disk swelling: Optic nerve swelling due to papilledema implies increased intracranial pressure and must be differentiated from swelling due to other causes, such as local inflammation (papillitis) and ischemic optic neuropathy. Papilledema is almost always bilateral, does not typically impair vision (except for enlargement of the blind spot), and is not associated with eye pain. Increased intracranial pressure is thought to cause papilledema by blocking axonal transport in the optic nerve. Because the optic nerve sheath communicates with the subarachnoid space, disorders associated with increased intracranial pressure that also obstruct the subarachnoid space, such as meningitis, are less likely to cause papilledema. In early papilledema, the retinal veins appear engorged and spontaneous venous pulsations are absent. The disk may be hyperemic, and linear hemorrhages may be seen at its borders. The disk margins become blurred, with the temporal edge last to be affected. In fully developed papilledema, the optic disk is elevated above the plane of the retina, and blood vessels crossing the border of the disk become obscured.

The findings of papilledema include:

Loss of venous pulsations

Swelling of the optic nerve head so there is loss of the disc margin

Venous engorgement

Disc hyperemia

Loss of the physiologic cup

Flame shaped hemorrhages.

Arteries & Veins: The caliber of the retinal arteries and veins should be observed where they arise from the disk and pass over its edges onto the retina. Features to note include whether these vessels are easily visible throughout their course, whether they appear engorged, and whether spontaneous venous pulsations (which indicate normal intracranial pressure) are present. The remainder of the visible retina is inspected, noting the presence of hemorrhages, exudates, or other abnormalities.

Macula: The macula, a somewhat paler area than the rest of the retina, is located approximately two disk diameters temporal to the temporal margin of the optic disk. It can be visualized quickly by having the patient look at the light from the ophthalmoscope. Ophthalmoscopic examination of the macula can reveal abnormalities related to visual loss from age-related macular degeneration, macular holes, or hereditary cerebromacular degenerations.

10
Q

CN 2 and 3

A

Pupils

In a brightly illuminated room, the diameter of normal pupils is approximately 3 mm in adults, smaller in the elderly, and greater than or equal to 5 mm in children. Pupil size may be asymmetric in up to 20% of people (physiologic anisocoria), but the difference is less than or equal to 1 mm. Symmetrically rapid constriction of the pupils in bright light indicates that pupillary function is normal and excludes oculomotor (III) nerve compression.

Pupillary Light Reflex

Direct (ipsilateral) and consensual (contralateral) pupillary constriction in response to a bright light shone in one eye demonstrates the integrity of the pathways.

The afferent or sensory limb of the pupillary light reflex is CN2

The efferent or motor limb is the parasympathetics of CN3.

#Swinging flashlight test #Relative Afferent Pupillary Defect #(Marcus Gunn Pupil) #(Gunn pupillary test)

Is used to test for a relative afferent pupillary defect or a Marcus Gunn pupil. Swinging the flashlight back and forth between the two eyes identifies if one pupil has less light perception than the other. Shine the flashlight at one eye noting the size of both pupils. Then swing the flashlight to the other eye. If both pupils now dilate then that eye has perceived less light stimulus (a defect in the sensory or afferent pathway) than the opposite eye.

Unilateral disorders of pupillary constriction are seen with local disease of the iris (trauma, iritis, glaucoma), oculomotor (III) nerve compression (tumor, aneurysm), administration of a mydriatic agent, and optic nerve disorders (optic neuritis, multiple sclerosis).

Reaction to accommofdation

When the eyes converge to focus on a nearer object (accommodation), the pupils normally constrict.

Supranuclear Gaze Systems

The purpose of supranuclear control of gaze is to insure that the image that is being looked at is centered or maintained on the fovea of the retina.

Eye movements are controlled by 4 major oculomotor gaze systems:

Saccades are tested by holding up your two hands about three feet apart and instructing the patient to “look at the finger that is wiggling without moving their head”. The patient’s eyes should be able to quickly, smoothly and accurately jump from target to target.

Pathway: Frontal gaze center to PPRF (paramedian pontine reticular formation)

Smooth Pursuit Tested with extraocular movements. The eyes should be able to follow the target smoothly without lagging behind or jerking to catch up with the target.

Pathway: Parietal-occipital gaze center via cerebellar and vestibular pathways.

The vestibulo-ocular reflex is obtained by having the patient visually fixate on an object straight ahead, then rapidly turning the patient’s head from side to side and up and down. The eyes should stay fixed on the object and turn in the opposite direction of the head movement.

Pathway: Vestibular input keeps image steady on fovea during head movements.

Vergence eye movements occur when the eyes move simultaneously inward (convergence) or outward (divergence) in order to maintain the image on the fovea that is close up or far away. Most often convergence is tested as part of the near triad. When a patient is asked to follow an object that is brought from a distance to the tip of their nose the eyes should converge, the pupil will constrict and the lens will roundup (accommodation).

Pathway: Optic to oculomotor nuclei to keep image on fovea predominantly when the viewed object is moved near (near triad- convergence, accommodation and pupillary constriction).

Nystagmus is a rhythmic oscillation of the eyes. Vestibular lesions result in a slow drift of the eyes away from the target in one direction (smooth pursuit), followed by a fast corrective movement (saccadic; fast phase) in the reverse direction that serves to bring the eye back on target. The eyes appear to “beat” in the direction of the fast phase.

Optokinetic Nystagmus is a test of smooth pursuit with quick resetting saccades. Use a tape with repeating shapes on it and ask the patient to look at each new object as it appears as you run the tape between your fingers to the right, left, up, and down. The patient will have brief pursuit eye movements in the direction of the tape movement with quick saccades or jerks in the opposite direction. The resetting saccades are easier to observe than the brief pursuit movement.

Nystagmus: Periphereal Lesion

Type: mixed horizontal-torsional nystagmus results if a peripheral lesion affects all three semicircular canals on one side. The horizontal fast phases beat toward the normal ear, as do the upper poles of the eyes for the torsional fast phases. The nystagmus from peripheral disease occasionally appears purely horizontal, never purely torsional or vertical.

Visual fixation: tends to suppress nystagmus that is due to a peripheral lesion, but it does not usually suppress nystagmus from a central lesion (use Frenzel lenses). The effect of fixation can also be determined during ophthalmoscopy if the examiner covers and uncovers the other eye.

Direction: In peripheral lesions, the predominant direction of nystagmus remains the same in all directions of gaze.

Deficient vestibuloocular reflex (VOR) implies a peripheral vestibular lesion (inner ear or vestibular nerve).

Nystagmus: Central Lesion

Direction: Nystagmus that reverses direction when the patient looks right then left suggests a central abnormality. Nystagmus that reverses direction with convergence also suggests a central lesion.

Other neurologic signs: the presence of additional neurologic abnormalities strongly suggests the presence of a central lesion.

11
Q

CN 3 and 4

A

Before checking ocular movements it is important to inspect the eyes:

Inspection and Ocular Alignment

Eyelid drooping (ptosis), pupil size, shape. Note the appearance of the eyes and check for ocular alignment (the reflection of your light source should fall on the same location of each eyeball).

These cranial nerves give us a view of the midbrain. The 3rd nerve in particular can give important anatomical localization because it exits the midbrain just medial to the cerebral peduncle.

The 3rd nerve controls eye adduction (medial rectus), elevation (superior rectus), depression (inferior rectus), up and in (inferior oblique), elevation of the eyelid (levator palpebrae superioris), and parasympathetics for the pupil.

CN III has 2 major components as follows:

Inner somatic fibers - innervate the levator muscle of the eyelid and 4 of the extraocular muscles (EOMs) (superior rectus, medial rectus, inferior rectus, inferior oblique). Because the inner somatic fibers are farther from the blood supply, they are more susceptible to ischemic injury. Therefore, patients with ischemic CN III palsy typically have paralysis of the levator muscle (ptosis) and 4 EOMs (“down-and-out-gaze”) with preserved pupillary response.

Superficial parasympathetic fibers - innervate the sphincter of the iris and the ciliary muscles (controlling pupil dilation).

The 4th nerve supplies the superior oblique muscle, which is important to looking down and in (towards the midline).

Versions

Testing extraocular range of motion with both eyes open and following the target (conjugate gaze) is called versions. The patient is asked to follow a target through the six principal positions of gaze.

Note any misalignment of the eyes or complaint of diplopia (double vision).

Ductions

If there is any misalignment of the eyes or diplopia on versions it is important to then examine each eye with the other covered (this is called ductions). The patient should follow an object through the six principle positions of gaze so each extraocular muscle function is tested.

isolated oculomotor (III) (or trochlear (IV) or abducens) (VI) nerve lesion may occur in patients with diabetes mellitus; noninvasive imaging procedures (CT scanning or MRI) reveal no abnormality.

Diabetic oculomotor (III) nerve lesions are characterized by pupillary sparing,
which is commonly attributed to infarction of the central portion of the nerve with sparing of the more peripherally situated fibers that mediate pupillary constriction. Pupilsparing oculomotor palsies also can be seen with compressive, infiltrative, or inflammatory lesions of the oculomotor
(III) nerve or with infarcts, hemorrhages, or tumors that affect the oculomotor (III) nucleus or fascicle within the midbrain. Pain, when present, may be severe enough to suggest aneurysmal expansion as a likely diagnosis.
12
Q

CN 5

A

The entry zone for this cranial nerve is at the mid pons with the motor and main sensory (discriminatory touch) nucleus located at the same level. The axons for the descending tract of the 5th nerve (pain and temperature) descend to the level of the upper cervical spinal cord before they synapse with neurons of the nucleus of the descending tract of the 5th nerve. Second order neurons then cross over and ascend to the VPM of the thalamus.

Sensory division: light touch (ophthalmic, mandibular, maxillary), pain (sharp)

Motor division: supplies the muscles of mastication (temporalis, masseter, and pterygoids). Palpate the temporalis and masseter muscles as the patient bites down hard. Then have the patient open their mouth and resist the examiner’s attempt to close the mouth. If there is weakness of the pterygoids the jaw will deviate towards the side of the weakness. The last test for this nerve is testing for a jaw jerk, which is a stretch reflex. Have the patient slightly open their mouth then place your finger on their chin and strike your finger with a reflex hammer. Normally there is no movement. If there is a jaw jerk it is said to be positive and this indicates an upper motor neuron lesion.

The ophthalmic division (V1) of the 5th nerve is the sensory or afferent limb and a branch of the 7th nerve to the orbicularis oculi muscle is the motor or efferent limb of the corneal reflex. The limbal junction of the cornea is lightly touched with a strand of cotton. The patient is asked if they feel the touch as well as the examiner observing the reflex blink.

13
Q

CN 6

A

This cranial nerve innervates the lateral rectus for eye abduction.

Remember that cranial nerves 3, 4 and 6 must work in concert for conjugate eye movements; if they don’t then diplopia (double vision) results.

The medial longitudinal fasciculus (MLF) connects the 6th nerve nucleus to the 3rd nerve nucleus for conjugate movement. A 6th nerve palsy may be a “false localizing sign”. The reason for this is that it has the longest intracranial route of the cranial nerves, therefore it is the most susceptible to pressure that can occur with any cause of increased intracranial pressure.

Rules of Diplopia:

Diplopia is maximum in the direction of action of the paretic muscle

The most peripherally seen image is the false image and comes from the eye with the paretic muscle.

The diplopia is horizontal if the medial or lateral recti are involved and vertical if the elevator or depressor muscles are involved.

Internuclear ophthalmoplegia (INO) A lesion of the MLF causes nystagmus of the abducting eye with absent adduction of the other eye. The lesion is on the side of the eye that should be adducting. There can be a bilateral INO in which case neither eye adducts with horizontal gaze.

14
Q

CN7

A

The motor division of CN 7 supplies the muscles of facial expression. Start from the top and work down. Have the patient wrinkle forehead (frontalis muscle), close eyes tight (orbicularis oculi) show their teeth (buccinator), and purse lips or blow a kiss (orbicularis oris), show teeth (looking at nasolabial folds); kiss or blow (orbicularis oris), puff cheeks (air escape). If there is weakness especially in a bilateral upper motor neuron distribution, get the patient to smile by telling a joke or funny story. With a pseudobulbar palsy automatic or emotional facial expression will be more complete than movements to command.

This cranial nerve has a motor component for muscles of facial expression (and, don’t forget, the stapedius muscle which is important for the acoustic reflex), parasympathetics for tear and salivary glands, and sensory for taste (anterior two-thirds of the tongue).

#Central (upper motor neuron-UMN) vs

#Peripheral (lower motor neuron-LMN)

7th nerve weakness: with a peripheral 7th nerve lesion all of the muscles ipsilateral to the affected nerve will be weak whereas with a “central 7th “, only the muscles of the lower half of the face contralateral to the lesion will be weak because the portion of the 7th nerve nucleus that supplies the upper face receives bilateral corticobulbar (UMN) input.

Taste is the sensory modality tested for the sensory division of CN 7. The examiner can use a cotton tip applicator dipped in a solution that is sweet, salty, sour, or bitter. Apply to one side then the other side of the extended tongue and have the patient decide on the taste before they pull their tongue back in to tell you their answer.

15
Q

CN 8

A

The cochlear division of CN 8 is tested by screening for auditory acuity. This can be done by the examiner lightly rubbing their fingers by each ear or by using a ticking watch. Compare right versus left. Further screening for conduction versus neurosensory hearing loss can be accomplished by using the Weber and Rinne tests.

The Weber test consists of placing a vibrating tuning fork on the middle of the head and asking if the patient feels or hears it best on one side or the other. The normal patient will say it is the same in both ears. The patient with unilateral neurosensory hearing loss will hear it best in the normal ear while the patient with a unilateral conductive hearing loss will hear it best in the abnormal ear.

Causes of sensorineural hearing loss:

Presbycusis

Ménière disease

Barotrauma (shooting a rifle w/o ear protection)

Acoustic neuroma

Cerebrovascular ischemia

The Rinne test consists of comparing bone conduction (placing the tuning fork on the mastoid process) versus air conduction (placing the tuning fork in front of the pinna). Normally, air conduction is greater than bone conduction. For neurosensory hearing loss air conduction is still greater than bone conduction but for conduction hearing loss bone conduction will be greater than air conduction.

The normal bilateral Rinne test response indicates there is not a conductive hearing loss on either side.

If conductive hearing loss in the right ear: The Weber test lateralizes to the right ear and bone conduction is greater than air conduction on the right.

Causes of conductive loss:

Otitis externa or media

Cholesteatoma

Trauma

Cerumen

Tympanic membrane rupture (hearing changes from altitude or from airplane travel are usually due to failure to equalize middle ear pressure)

This nerve is a sensory nerve with two divisions- acoustic and vestibular. The acoustic division is tested by checking auditory acuity and with the Rinne and Weber tests.

The vestibular division of this nerve is important for balance. Clinically it be tested with the oculocephalic reflex (Doll’s eye maneuver) and oculovestibular reflex (ice water calorics).

Dix-Hallpike (turn patients head to 45 degrees, bring them down into slight extension). or half-somersault or Epley

16
Q

CN 9 and 10

A

The motor division of CN 9 (Glossopharyngeal) & 10 (Vagus) is tested by having the patient say “ah” or “kah”. The palate should rise symmetrically and there should be little nasal air escape. With unilateral weakness the uvula will deviate toward the normal side because that side of the palate is pulled up higher. With bilateral weakness neither side of the palate will elevate and there will be marked nasal air escape.

These two nerves are clinically lumped together. Motor wise, they innervate pharyngeal and laryngeal muscles. Their sensory component is sensation for the pharynx and taste for the posterior one-third of the tongue.

“Say kuh kuh kuh, say ah (nasal air escape)(action of palate); gag reflex”

17
Q

CN 11

A

Spinal Accessory: This nerve is a motor nerve for the sternocleidomastoid and trapezius muscles. The UMN control for the sternocleidomastoid (SCM) is an exception to the rule of the ipsilateral cerebral hemisphere controls the movement of the contralateral side of the body. Because of the crossing then recrossing of the corticobulbar tracts at the high cervical level, the ipsilateral cerebral hemisphere controls the ipsilateral SCM muscle. This makes sense as far as coordinating head movement with body movement if you think about it (remember that the SCM turns the head to the opposite side). So if I want to work with the left side of my body I would want to turn my head to the left so the right SCM would be activated.

“turn head and shrug shoulders against my force”

18
Q

CN 12 - Motor

A

Hypoglossal: The 12th CN is tested by having the patient stick out their tongue and move it side to side. Further strength testing can be done by having the patient push the tongue against a tongue blade. Inspect the tongue for atrophy and fasciculations. If there is unilateral weakness, the protruded tongue will deviate towards the weak side.

By having the patient say lah-pah-kah, the examiner is testing the motor components of CN 12, 7, and 9 & 10.

Tongue movement and stretch (in and out; side to side) La, la, la; Pa, Pa, Pa (7) kuh kuh kuh (9 and 10)[tongue fasciculations]

19
Q

Sensory

A

Light touch (close eyes and tell me when I touch you “say yes”) any difference?

Sharp, prick (Is this sharp different)[“tell me when it feels like a normal thigh area”]

Position/proprioception (finger down or up)[“look away”], rhomberg (tap the person)[rhomberg with sway]

Tactile movement

20
Q

Motor

A

Muscle Appearance:

Wasting, or muscle atrophy, suggests that weakness is due to a lesion of the lower motor neurons or the muscle itself.

Fasciculations—visible irregular flickerings over the surface of the affected muscle caused by spontaneous contractions of individual motor units—suggest that weakness is due to a lower motor neuron lesion.

Flexor or extensor spasms of the limbs are sometimes seen in upper motor neuron disorders as a result of impaired supraspinal control of reflex activity.

Muscle Tone:

Tone can be defined as the resistance of muscle to passive movement of a joint. Tone is assessed by observing the position of the extremities at rest, by palpating the muscle belly, and particularly by determining the resistance to passive stretch and movement. To assess resistance to passive movement, the patient relaxes while each limb is examined in turn by passively taking the major joints through their full range of movement at different speeds and estimating whether the force required is more or less than normal. “I’m going to wiggle your arm”.

Spasticity: The resistance of an affected muscle is not the same throughout the range of movement, but tends to be most marked when passive movement is initiated and then diminishes as the movement continues (the clasp-knife phenomenon). Spasticity is caused by an upper motor neuron lesion, such as a stroke that involves the supplementary motor cortex or corticospinal tract.

Rigidity: consists of increased resistance to passive movement that is independent of the direction of the movement; that is, it affects agonist and antagonist muscle groups equally (lead-pipe rigidity). The term cogwheel rigidity is used when there are superimposed ratchet-like interruptions in the passive movement, probably related to underlying tremor. In general, rigidity indicates extrapyramidal dysfunction and is due to a lesion of the basal ganglia (eg, Parkinson disease).

Hypotonia (flaccidity): This is characterized by excessive floppinessa reduced resistance to passive movement—so that the distal portion of the limb is easily waved to and fro when the extremity is passively shaken. In hypotonic limbs it is often possible to hyperextend the joints, and the muscle belly may look flattened and feel less firm than usual. Although hypotonia usually relates to pathologic involvement of the lower motor neuron supply to the affected muscles, it can also occur with primary muscle disorders, disruption of the sensory (afferent) limb of the reflex arc, cerebellar disease, and certain extrapyramidal disorders such as Huntington disease, as well as in the acute stage of a pyramidal lesion.

Shoulder ROM: forward flexion, abduction, external rotation, Internal rotation (thumbs up spine), Neer’s impingement, supraspinatus strength (thumbs down), infraspinatus strength (push in/our), palpate deltoid, bicep, triceps (C7) , bicep strength (C6),

Elbow ROM (flexion, extension, pronation, supination), tinels, provocative test, grip test, wrist (C8) - forced wrist extension.

Hand ROM – hands (spread) - radial ulnar styloid process, thumb adductor, snuff, thenar muscle mass flexion (roof), PIP, DIP, extension, opposition, tinels sign (medial cubital fossa), phalens sign.

Lower Extremity ROM: Wiggle (clonus?, “complete and full”), Illopsoas (L2), adductors, abductors, quads (L3), hamstrings (L5), anterior tibial (L5), plantarflex (S1), posterior tibs, peroneal.

Squat and rise, heel and toe walking

Localization of the Underlying Lesion

Voluntary muscle activity is mediated by the corticospinal (pyramidal) tracts. First-order neurons of these tracts are located in the premotor and motor cortex of the frontal lobe (Brodmann areas 6 and 4, respectively). Their efferent fibers descend through the internal capsule, midbrain, and pons, and continue to form the pyramids on the anterior aspect of the medulla. In the medulla, 90% of the fibers decussate (cross) to form the lateral corticospinal tract. Fibers that do not decussate descend as the anterior corticospinal tract. The axons of both tracts synapse on the motor neurons of the anterior horn (second-order neurons). Damage to the corticospinal tract is divided into upper and lower motor neuron lesions:

Upper motor neuron (UMN) refers to anything above the anterior horn (spinal cord). Lesions to UMNs (eg, due to stroke, brain tumor) cause a combination of “pyramidal signs”: spastic paralysis, clasp-knife rigidity (characterized by initial resistance to passive extension followed by a sudden release of resistance),

Weakness or paralysis

Increased tendon reflexes

Spasticity (Clasp-knife spasticity and spastic paralysis) occurs within the flexors of the upper limb and the extensors of the lower limb. There is a sudden decrease in resistance (often termed a “release”) when attempting to flex a joint.

Hyperreflexia (including clonus), and upgoing plantar reflexes (Babinski sign). This likely occurs due to loss of descending inhibition over second-order neurons in the anterior horn. Babinski sign indicates an upper motor neuron (UMN) lesion anywhere along the corticospinal tract. UMNs are thought to have inhibitory control over lower motor neurons (LMN), thus removal of UMN input causes overstimulation of LMNs and leads to unmasking of primitive reflexes, such as the Babinski reflex.

Pronator drift: patient holds arms extended, palms up, and eyes closed. Slight inward drifting rotation (pronation) of one forearm or a curling of fingertips is abnormal. Abnormal findings indicate a contralateral pyramidal tract lesion.

Lower motor neuron (LMN) refers to motor neurons of the anterior horn. This type of injury leads to flaccid paralysis, hypotonia, hyporeflexia, muscle atrophy, and fasciculations.

Weakness or paralysis

Fasciculations are involuntary muscle contractions that arise from the spontaneous discharge of muscle fibers or motor units. They are a sign of LMN disease

Flaccid Paralysis (ie. bladder) typically occurs in the setting of lower motor neuron lesions (cauda equina syndrome). A patient with a flaccid bladder will have a large residual volume of urine after attempted emptying and will typically experience urinary incontinence at the end of the day (pressure from a full bladder becomes greater than urinary sphincter pressure).

Muscle atrophy

Hypotonia

Combined UMN and LMN lesions are characteristic of amyotrophic lateral sclerosis (Lou Gehrig disease).

ALS: Degeneration of the corticospinal tracts (leading to upper motor neuron signs) and degeneration of the anterior roots of the spinal cord (leading to lower motor neuron signs). No bowel or bladder deficits are seen

Tx: Riluzole works by blocking glutamatergic neurotransmission by inhibition of glutamate release and inactivation of voltage-gated Na channels. You give Riluzole for Lou Gehrig Disease. Autosomal dominant mutations in superoxide dismutase type 1 (SOD1) are a cause of familial ALS.

  • *5** Normal power
  • *4** Active movement against resistance and gravity
  • *3** Active movement against gravity but not resistance
  • *2** Active movement possible only with gravity eliminated
  • *1 Flicker** or trace of contraction
  • *0** No contraction

Tremor a rhythmic oscillatory movement best characterized by its relationship to voluntary motor activity, that is, according to whether it occurs at rest, during maintenance of a particular posture, or during movement. Enhanced by emotional stress and disappears during sleep.

Tremor that occurs when the limb is at rest is generally referred to as static tremor or rest tremor.

Physiologic Tremor: An 8- to 12-Hz tremor of the outstretched hands is a normal finding.

Intention or kinetic tremor occurs during activity; results from a lesion affecting the superior cerebellar peduncle.

Chorea denotes rapid irregular muscle jerks that occur involuntarily and unpredictably in different parts of the body. Power is full, but there may be difficulty in maintaining muscular contraction such that, for example, handgrip is relaxed intermittently (milkmaid grasp). The gait becomes irregular and unsteady, with the patient suddenly dipping or lurching to one side or the other (dancing gait). Speech often becomes irregular in volume and tempo and may be explosive in character. Chorea disappears during sleep. Some cases are associated with cell loss in the caudate nucleus and putamen.

Hemiballismus is unilateral chorea that is especially violent because the proximal muscles of the limbs are involved. It is due most often to vascular disease in the contralateral subthalamic nucleus and commonly resolves spontaneously in the weeks after its onset.

Athetosis generally denotes abnormal movements that are slow, sinuous, and writhing in character. When the movements are so sustained that they are better regarded as abnormal postures, the term dystonia is used, and many now use the terms interchangeably. Excessive or inappropriate contraction of muscles (often agonists and antagonists) leads to sustained abnormal postures of the affected region of the body. The abnormal movements and postures may be generalized (involving the trunk and at least two other sites) or restricted in distribution, such as to the neck (torticollis), hand and forearm (writer’s cramp), or mouth (oromandibular dystonia). With restricted dystonias, two or more contiguous body regions (eg, upper and lower face) may be affected (segmental dystonia), or the disturbance may be limited to localized muscle groups so that only a single body region is involved (focal dystonia).

Myoclonic jerks are sudden, rapid, twitchlike muscle contractions. Generalized myoclonus has a widespread distribution, whereas focal or segmental myoclonus is restricted to a particular part of the body. Myoclonus can be spontaneous, or it can be brought on by sensory stimulation, arousal, or the initiation of movement (action myoclonus). Myoclonus may occur as a normal phenomenon (physiologic myoclonus) in healthy persons, as an isolated abnormality (essential myoclonus), or as a manifestation of epilepsy (epileptic myoclonus). It can also occur as a feature of a variety of degenerative, infectious, and metabolic disorders (symptomatic myoclonus) affecting the cerebral cortex, brainstem, or spinal cord. Myoclonus is sometimes manifest not by a sudden twitchlike muscle contraction but by a sudden loss of muscle activity (negative myoclonus). This is best seen as asterixis. Physiologic myoclonus includes the myoclonus that occurs upon falling asleep or awakening (nocturnal myoclonus) as well as hiccup…..

21
Q

Reflexes

A

Reflexes – (0-3)[2 is normal] triceps, brachioradialis, achilles, babinski

0, absent

1, reduced, trace response, or present only with reinforcement

2 and 3, in lower and upper half of normal range, respectively

4, increased, with or without clonus.

Hoffman sign, clonus, jaw jerk

Performance of the Jendrassik maneuver (an attempt by the patient to pull apart the fingers of the two hands when they are hooked together) or some similar distracting action (such as making a fist with the hand that is not being tested) may allow an otherwise unobtainable reflex response to be elicited.

Clonus consists of a series of rhythmic reflex contractions of a muscle that is suddenly subjected to sustained stretch, with each beat caused by renewed stretch of the muscle during relaxation from its previous contracted state.

Sustained clonus: more than three or four beats in response to sudden sustained stretch—is always pathologic and is associated with an abnormally brisk reflex.

Babinski: An extensor plantar response can also be elicited, though less reliably, by such maneuvers as pricking the dorsal surface of the big toe with a pin (Bing sign), firmly stroking down the anterior border of the tibia from knee to ankle (Oppenheim maneuver), squeezing the calf muscle (Gordon maneuver), or Achilles tendon (Schafer maneuver), flicking the little toe (Gonda maneuver), or stroking the back of the foot just below the lateral malleolus (Chaddock maneuver).

22
Q

Coordination and Gait

A

Coordination – rapid alternating movements, finger to nose, heel to shin.

Finger-to-nose: Under (hypometria) and over (hypermetria) shooting of a target (dysmetria) and the decomposition of movement (the breakdown of the movement into its parts with impaired timing and integration of muscle activity) are seen with appendicular ataxia.

Toe-to-finger: Same as finger-to-nose except for the lower extremities.

Heel-to-shin: The patient with ataxia of the lower extremity will have difficulty placing the heel on the knee with a side-to-side irregular over- and undershooting as the heel is advanced down the shin. Dysmetria on heel-to-shin can be seen in midline ataxia syndromes as well as cerebellar hemisphere disease so there is overlap between the two types of ataxias for this finding.

Rapid alternating movements: screw an imaginary light bulb into the ceiling with each arm in turn, and to rub the fingers of one hand in a circular polishing movement on the back of the other hand. Inability to perform repetitive movements in a rapid rhythmic fashion is called dysdiadochokinesia.

Vestibulocerebellum
The 1st subdivision is the vestibulocerebellum. This consists of the connections between the vestibular system and the flocculonodular lobe. Dysfunction of this system results in nystagmus, truncal instability (titubation), and truncal ataxia.

Station

Walking

Tandem gait

Spinocerebellum

The 2nd subdivision is the spinocerebellum. This system consists of the connections between the cutaneous and proprioceptive information coming from the spinal cord to the vermis and paravermis regions with corrective feedback predominantly to the muscles of truncal stability and gait. Dysfunction of this system results in gait and truncal ataxia.

Midline Ataxia

Clinically, the ataxic syndromes caused by vestibulocerebellar and spinocerebellar disease are lumped together and are called midline or equilibratory (gait) ataxias. The hallmarks of these midline ataxic syndromes are truncal instability manifested by titubation (tremor of the trunk in an anterior-posterior plane at 3-4 Hz) and gait ataxia (wide based, irregular steps with lateral veering).

Cerebrocerebellum

The 3rd subdivision of the cerebellum is the cerebrocerebellum. This system consists of connections from the cerebral cortex (predominantly motor) to the cerebellar hemispheres then back to the cerebral cortex. This system is important in motor planning.

It is important to remember that ataxia caused by disease of the cerebellar hemispheres will be ipsilateral to the dysfunctional hemisphere. The findings of appendicular ataxia are hypotonia, decomposition of movement, dysmetria, and difficulty with rapid alternating movements (dysdiadochokinesia):

A cerebellar intention tremor arises mainly from limb girdle muscles and is maximal at the most demanding phase of the active movement. This must be distinguished from a postural tremor (fine distal 8-13 Hz)(2nd scene) or resting tremor (coarse distal 5-6 Hz pill-rolling type of tremor)(3rd scene).

Gait

Station: Patient’s feet will be placed wider apart then usual in order to maintain balance (broad or wide-based station). Midline ataxias cause instability of station with eyes opened or closed.

Natural Gait: Wide-based, unsteady, irregular steps with lateral veering; ataxia is most prominent when sudden changes are needed such as turning, standing up or stopping.

toe walking, heel walking (strength)

Tandem gait: Patients with ataxia have difficulty narrowing the station in order to walk heel to toe. Tandem gait is helpful in identifying subtle or mild gait ataxia.

Rhomberg: The patient assumes a steady stance with feet together, arms oustretched, and eyes closed and is observed for any tendency to sway or fall. The test is positive (abnormal) if unsteadiness is markedly increased by eye closure—as occurs, for example, in tabes dorsalis. A positive test is indicative of grossly impaired joint position sense in the legs.