Fig. 6D(v).31: Rooting reflex.

Fig. 6D(v).32: Pout reflex. Fig. 6D(v).33: Grasp reflex.

INVERTED AND PERVERTED REFLEXES

Reflex Description and example

Inverted

reflex

Contractions opposite to that of expected

For example:

An inverted brachioradialis reflex: When the supinator reflex elicits finger flexion and not elbow flexion

Is associated with an absent biceps jerk and an exaggerated triceps jerk

Is indicative of a spinal cord lesion at C5 or C6, e.g. due to trauma, syringomyelia, or disc prolapse

Inversion of biceps reflex

On eliciting bicep reflex the following are noticed:

There is no flexion at the elbow

But instead there is extension at the elbow due contraction of the triceps muscle

Presence of this reflex indicates that the lesion is at the level of C5 segment

Inversion of triceps reflex With disc protrusions at C6/7 there is a “paradoxical triceps reflex” with forearm muscles acting to flex the elbow

against no triceps resistance

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Inversion of knee reflex

On eliciting the knee jerk

There is no extension of the knee joint

But instead there is flexion of the knee due to contraction of the hamstring muscles

Presence of this indicates that the lesion is at the level of L3, 4

Perverted

reflex

It is false inverted reflex where there is an alteration in the response rather than true inversion

For example: When supinator jerk is elicited there is a perverted response of finger flexion. (Note: In the presence of

brachioradialis reflex this phenomenon is called as spread of reflex, while in the absent of brachioradialis reflex this is

considered as pseudo inverted reflex or perverted reflex)

Other Causes of Altered Reflexes

Thyroid disease Woltman’s sign of myxedema, is the delayed relaxation phase of the muscle stretch reflex.

In hypothermia or β-blockade, the relaxation phase of the ankle jerk may be prolonged.

Chorea: “Hung-up” knee jerk is a specific but rarely appreciated clinical sign of Huntington disease (HD) and Sydenham chorea.

During an elicited knee jerk, the extended lower leg may not relax immediately but may remain elevated for several seconds due

to sustained contraction of the quadriceps femoris.

Very brisk reflexes—even with a few beats of clonus can be seen in anxious individuals, as well as in hyperthyroidism and in

tetany.

Electrolyte disturbances

Absent reflexes is seen with hypermagnesemia.

In the Holmes Adie syndrome, absent deep tendon reflexes are seen.

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D(vi). SENSORY SYSTEM EXAMINATION

SENSORY SYSTEM EXAMINATION

Sensations can be grossly divided into primary and secondary modalities

Primary modalities Secondary modalities (cortical sensation)

Touch

Pressure

Pain

Temperature

Joint position sense

Vibration

Tactile localization

2 point discrimination

Sensory inattention

Stereognosis

Graphesthesia

These require secondary association area in parietal lobe

Note: When primary sensation are normal but secondary modalities are lost it implies a parietal lobe

lesion.

Sherrington classification of sensory system

Exteroceptive

system

Information about the external environment, including somatosensory functions and special senses

Proprioceptive

system

Senses the orientation of the limbs and body in space

Interoceptive system Information about internal functions, blood pressure, or the concentration of chemical constituents in

bodily fluids

PRIMARY MODALITIES

Examination of Exteroceptive System (Spinothalamic Tract)

Pain

Ask the patient to close his eyes.

Sharp end of pin is applied mildly sufficient to produce pain but not to penetrate the skin [Fig.

6D(vi).1].

Compare adjacent normal area and corresponding area on the opposite side.

Indicate whether sensation is normal, decreased (or absent) or increased.

In peripheral nerve disease, there is anesthesia more than analgesia.

In spinal cord disease, there is analgesia more than anesthesia.

Commonly used objects are the safety pin or broken wooden applicator stick.

Avoid too sharp objects and hypodermic needles.

A useful trick is to hold the pin or shaft of the applicator stick lightly between thumb and fingertip and

allow the shaft to slide between fingertip and thumb. This ensures consistent stimulus intensity.

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Fig. 6D(vi).1: Examination of pin prick sensation.

Temperature [Fig. 6D(vi).2]

With the patient’s eyes closed, apply the warm and cold test tubes randomly over the skin in

dermatomal pattern.

Instruct the patient to say what he feels–hot/cold/no response.

Cold = 5°C to 10°C (41°F to 50°F) (crushed ice can be used). Warmth = 40°C to 45°C (104°F to 113°F) (warm water can be used).

Temperature much lower or higher than these elicit pain rather than temperature sensations.

In lesions of leprosy, temperature may be lost prior to pain.

Fig. 6D(vi).2: Examination of temperature.

Tactile Sensation

Light touch can be tested with a:

Wisp of cotton [Fig. 6D(vi).3]

Feather

Soft brush [Fig. 6D(vi).4]

Light touch of the fingertip.

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For diabetic neuropathies

Von Grey’s hairs

Semmelweis monofilament

With patient’s eyes closed, gently touch the skin (preferably non-hairy region) without exerting

pressure.

Ask the patient whether he can feel the touch.

Tactile response can be graded as per international spinal injury standards as

0 = absent

1 = altered response (impaired/increased)

2 = normal/intact response.

Fig. 6D(vi).3: Examination of tactile sensation with wisp of cotton.

Fig 6D.vi.4: Examination of tactile sensation with soft brush.

Examination of Proprioceptive System

Proprioception (Proprioception refers to either the sense of position of a body part or motion of a body part)

Conscious component Unconscious component

Travels with the fibers subserving fine, discriminative touch. Via spinocerebellar tract

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These include:

Motion

Position

Vibration

Pressure

Examination of different components of proprioception: Joint motion and position:

Usually tested together

In the lower extremity [Figs. 6D(vi).5A and B]:

Tested at the metatarsophalangeal joint of the great toe,

In the upper extremity [Figs. 6D(vi).6A to C]:

At one of the distal interphalangeal joints. If these distal joints are normal, there is no need to test

more proximally.

Joint motion:

Testing is done with the patient’s eyes closed.

It is extremely helpful to instruct the patient, eyes open, about the responses expected before

beginning the test.

Show the patient up or down movements and instruct him to reply “up” or “down”.

The examiner should hold the patient’s completely relaxed digit on the sides, away from the

neighboring digits, parallel to the plane of movement, exerting as little pressure as possible to

eliminate clues from variations in pressure.

The part is then passively moved up or down, and the patient is instructed to indicate the direction of

movement from the last position.

Healthy young individuals can detect great toe movements of about 1 mm, or 2° to 3°; and in the

fingers virtually invisible movements, 1° or less, at the distal interphalangeal joint are accurately

detected.

Figs. 6D(vi).5A and B: Examination of joint sense in the lower limb.

Figs. 6D(vi).6A to C: Examination of joint sense in upper limb.

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Position sense:

Tested by placing the fingers of one of the patient’s hands in a certain position (like “OK” sign) [Fig.

6D(vi).7] while his eyes are closed, and then asking him to imitate it with the other hand OR do

passive movement in one hand and ask the patient to do in similar way in other hand [Fig. 6D(vi).8].

This is sometimes referred to as parietal copy. Light touch can be tested with a wisp of cotton, tissue

paper, a feather, a soft brush, light stroking of the hairs, or even using a very light touch of the

fingertip. Both parietal lobes (and their connections) must be intact: one side to register the position

and the other side to copy it.

Vibration (pallesthesia) [Figs. 6D(vi).9A to C]: Preferentially using a tuning fork of 128Hz due to slow

decay (256 Hz is used to detect early changes in cases like subacute combined cord degeneration).

Fig. 6D(vi).7: Examination of position sense (OK sign).

Explain procedure to patient clearly.

Strike the tuning fork and place on the forehead and explain the difference between vibration and

plain touch of tuning fork, by dampening the vibration by holding the prongs.

Fig. 6D(vi).8: Examination of position sense by asking to copy passive movement.

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Fig. 6D(vi).9A: Demonstration of vibration over proximal great toe.

Fig. 6D(vi).9B: Demonstration of vibration over medial malleolus.

Keep the vibrating tuning fork, starting from the distal most bony prominence and proceed proximally.

Ask the patient to say when he ceases to feel the vibration.

Timed vibration test:

It is the most sensitive and simple method to quantify defects in vibration.

Note the time duration of perception of vibration after the tuning fork is set into vibration.

Normally

≥10 sec in lower limb.

≥20 sec in upper limb.

Rhomberg’s sign [Figs. 6D(vi).10A and B]:

It is a sign of posterior column dysfunction.

Ask the patient to stand upright with feet/heels close together, arms by the side and eyes open.

Any significant swaying is noted.

Now, ask the patient to close the eyes while taking adequate measures to make sure patient does not

fall and hurt himself. Watch for swaying

Minimal swaying is normal.

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Immediate gross swaying is considered as positive test.

Pseudoathetosis [Fig. 6D(vi).11]:

It is an upper limb equivalent of examination of posterior column dysfunction.

Ask the patient to hold the upper limb in extended position and close the eyes. Watch for slow writhing movements of fingers (piano-playing movement) which disappear on opening

the eyes.

Pressure pain:

Tested by squeezing the Achilles tendon or calf muscle.

Abadie’s sign is loss of deep pain (seen with diseases affecting the posterior column like

neurosyphilis–tabes dorsalis).

Fig. 6D(vi).9C: Demonstration of vibration over the proximal 1st metacarpopharyngeal joint.

Figs. 6D(vi).10A and B: Demonstration of Rhomberg’s sign.

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Fig. 6D(vi).11: Demonstration of pseudoathetosis in upper limb.

SECONDARY MODALITIES

Cortical Sensations

Cortical sensations cannot reliably be tested unless primary sensation is intact bilaterally.

Two-point discrimination [Fig. 6D(vi).12]: Ability to recognize simultaneous stimulation by two blunt

points. Measured by the distance between the points required for recognition. The normal distances at

which two points can be discriminated on various body parts:

Tongue tip: 1 mm

Fingertip: 2 to 4 mm

Dorsum of fingers: 4 to 6 mm

Palm: 8 to 12 mm

Dorsum of hand: 20 to 30 mm

Skin over the back : 30–40 mm.

Tactile localization (topognosis):

Ability to localize stimuli to parts of the body. Topagnosia is the absence of this ability.

Graphesthesia [Fig. 6D(vi).13]:

Ask the patient to close their eyes and identify letters or numbers that are being traced onto their palm

or the tip of their finger.

Stereognosis [Figs. 6D(vi).14A and B]:

Ask the patient to close their eyes and identify various objects by touch using one hand at a time.

Tactile extinction (double simultaneous stimulation) [Figs. 6D(vi).15A and B]

Ability to perceive a sensory stimulus when corresponding areas on the opposite side of the body are

stimulated simultaneously. Loss of this ability is termed sensory extinction (perceptual rivalry/sensory

suppression).

The site of lesion is contralateral parietal lobe.

Fig. 6D(vi).12: Demonstration of 2 point discrimination.

Fig. 6D(vi).13: Demonstration of graphesthesia.

Fig. 6D(vi).14A: Demonstration of stereognosis with key.

Fig. 6D(vi).14B: Demonstration of stereognosis with coin.

Fig. 6D(vi).15A: Demonstration of tactile extinction in upper limb. Fig. 6D(vi).15B: Demonstration of tactile extinction in lower lim

Disorders of touch

Anesthesia Absence of touch appreciation.

Hypoesthesia Decrease in touch appreciation.

Hyperesthesia Exaggeration of touch sensation, which is often unpleasant.

Paresthesia Abnormal sensations perceived without specific stimulation. They can include wide variety of

abnormal sensation except pain; episodic or constant.

Hyperpathia Exaggerated reaction to any stimuli (touch/pressure/pain).

Disorders of pain

Analgesia Absence of pain appreciation.

Hypoalgesia Decrease in pain appreciation.

Hyperalgesia Exaggeration of pain appreciation, which is often unpleasant.

Allodynia Perception of non-painful stimulus as painful.

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Causalgia Persistent pain, allodynia or hyperalgesia along with abnormal pseudomotor activity (edema and

blood flow changes). It is also called as reflex sympathetic dystrophy.

Phantom limb pain Individuals who have had a limb amputated may experience pain or tingling sensations that feels

as if they were coming from the amputated limb, just as if that limb were still present. These

individuals experience pain or tingling sensations that feel as if they were coming from the

amputated limb, just as if that limb were still present.

Central or thalamic pain Spontaneous, inexplicable, agonizing pain and other unusual sensations in the anesthetic parts.

Disorders of temperature

Thermanalgesia Absence of temperature appreciation

Thermhypoesthesia Decrease of temperature appreciation

Thermhyperesthesia Exaggeration of temperature sensation, which is often unpleasant

Disorders of posterior column sensations

Arthranesthesia Absence of joint position sense (Arthresthesia—perception of joint position sense)

Apallesthesia/Pallanesthesia Absence of vibration sense

Barognosis (recognition of weight)

The ability to recognize different weights.

A set of discrimination weights consisting of small objects of the same size and shape but of

graduated weights are used.

HOMUNCULUS, SENSORY PATHWAY, DERMATOMES AND CLINICAL

PATTERNS OF SENSORY LOSS

Fig. 6D(vi).16: Sensory homunculus.

Fig. 6D(vi).17: Sensory pathway.

Sensation Receptor Pathway Decussation

Pain and thermal sense from the body Aδ and C fiber endings Spinothalamic tract

of anterolateral

system (ALS)

Anterior

white

commissure

Nondiscriminative (crude) touch and

superficial pressure from the body

Free nerve endings, Merkel’s disks,

peritrichial nerve endings

Spinothalamic tract

of ALS

Anterior

white

commissure

Two-point discriminative (fine) touch,

vibratory sense, proprioceptive sense from

muscles and joints of body

Meissner’s corpuscles, Pacinian

corpuscles, muscle stretch receptors, Golgi tendon organs

First order fibers:

Fasciculi gracilis and

cuneatus

Second order fibers: Medial lemniscus

Medial

lemniscal

decussation

Fig. 6D(vi).18: Anterior view of skin segment innervation.

Fig. 6D(vi).19: Posterior view of skin segment innervation.

Figs. 6D(vi).20A to H: Clinical patterns of sensory dysfunction.

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D(vii). CEREBELLUM AND COORDINATION

SIGNS OF CEREBELLAR DISORDERS

Deficit Manifestation

Ataxia Reeling, wide-based gait.

Decomposition of movement

Inability to sequence fine, coordinate acts correctly.

This is usually tested while performing the finger-nose test which requires a fine coordination between

shoulder, elbow, and wrist joint. Patients with a cerebellar lesion will find it difficult to perform such movements.

Dysarthria Inability to articulate words correctly, usually manifesting as slurring and/or inappropriate phrasing.

Dysdiadochokinesia Inability to perform rapid, alternating movements.

Dysmetria Inability to control or limit the range of movement.

Hypotonia Decrease in muscle tone.

Nystagmus Involuntary rapid oscillation of eyeballs in a horizontal, vertical or rotationary fashion with the fast

component of nystagmus maximal towards the side of the cerebellar lesion.

Scanning/Staccato

speech

Slow explosive enunciation with a tendency to hesitate at the beginning of each word or each syllable.

Asking the patient to pronounce a word with multiple syllables, such as Mississippi or Venkataramana will

elicit distinct pauses before each syllable.

Tremor Rhythmic, alternating, oscillatory movements which affects a limb as it approaches a target (Intention

tremor) or of proximal musculature when attempting to bear weight (postural tremor).

Hypotonia

Usually accompanies acute hemispheric lesions.

Interestingly, it is seen less often in chronic lesions.

Ipsilateral to the side of a cerebellar lesion.

More noticeable in upper limbs and proximal muscles.

Pendular knee jerk: Leg keeps swinging after knee jerk more than 4 times (4 or less is considered normal).

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Ataxia

Defective timing of sequential contraction of agonist/antagonist muscles.

Results in a disturbance in smooth performance of voluntary acts (errors in rate, range, force, duration).

May affect limbs, trunk, gait (depends on the part of cerebellum involved).

Asynergia

Lack of synergy of various muscles while performing complex movements (movements are broken up into isolated, successive

parts. This is known as decomposition of movement).

Dysmetria OR abnormal excursions in movement

Finger-to-nose test

With eyes open, the patient is asked to partially extend elbow and rapidly bring tip of index finger in a wide arc to tip of his

nose.

In cerebellar disease, the action may manifest an intention tremor. With eyes closed, sense of position in the shoulder and elbow is tested.

Heel-to-shin test

Patient is asked to place one heel on opposite knee and slide the heel down the tibia with foot dorsiflexed.

Movement should be performed accurately.

In cerebellar disease, the arc of the movement is jerky/wavering.

The slide down the shin may manifest an action tremor.

Dysdiadochokinesia OR impaired performance of rapidly alternating movement

Normal coordination includes ability to arrest one motor impulse and substitute the opposite.

There are several simple clinical methods to test this:

Alternating movements (pronate and supinate forearm and hand quickly): In cerebellar disease, the movements tend to

overshoot or are inadequate resulting in irregular or inaccurate movements.

Rapidly tap fingers on the table.

Open and close fists.

Stewart-Holmes rebound sign.

Have the patient pull on your hand and when they do, slip your hand out of their grasp. Normally the antagonists muscles will

contract and stop their arm from moving in the desired direction. A positive sign is seen in a spastic limb where the exaggerated

“rebound” occurs with movement in the opposite direction. However, in cerebellar disease, this response is completely absent

causing the limb to continue moving in the desired direction. (Be careful that you protect the patient from the unrestricted movement causing them to strike themselves).

Past pointing

Overshoot is also commonly seen as part of ataxic movements and is sometimes referred to as past pointing, when the patient

overshoots while reaching target (finger-to-nose test)

Cerebellar dysarthria

Abnormalities in articulation and prosody (together or independent).

Scanning, slurring, staccato, explosive, hesitant, garbled speech.

Hemisphere lesions are associated with speech disorders more often than vermal lesions.

Causes enunciation of individual syllables: “the British Parliament” becomes “the Brit-tish Par-la-ment.”

Intention tremor—occurs during goal-directed movements. Intention tremor results when the antagonist activation that normally

stops a goal-directed movement as the goal is approached is inappropriately sized or timed.

Oculomotor dysfunction

Nystagmus frequently seen in cerebellar disorders.

Gaze-evoked nystagmus, upbeat nystagmus, rebound nystagmus, optokinetic nystagmus may all be seen in midline cerebellar

lesions.

Gait

In cerebellar disease, the gait is staggering/lurching/wavering.

Lesion in mid-cerebellum: Movements are in all directions.

Lesion in lateral cerebellum: Staggering/falling is toward the side of the lesion.

Somewhat steadied by standing or walking on a wide base.

Position of feet

Ataxia from cerebellar disease is less when the patient stands on a broad base (feet widely apart).

Eyes open or closed

Cerebellar ataxia is not improved by visual orientation; ataxia from posterior column disease (disordered proprioception) is

worsened with the eyes closed.

Direction of Falling

Disease of lateral lobe of cerebellum causes falling to ipsilateral side.

Lesions of midline/vermis cause indiscriminate falling depending on initial stance of the patient.

Titubation

Consists of a rhythmic body or head tremor. There is a rotatory, rocking or bobbing movement. Clinically, this does not have

significant value in localizing the lesion with respect to the part of the cerebellum involved.

HEEL KNEE TEST [FIGS. 6D(VII).1A TO D]

The 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.

Figs. 6D(vii).1A to D: Demonstration of heel knee test.

TOE FINGER TEST [FIGS. 6D(VII).2A AND B]

Patient lies in bed and is asked to touch his great toe to the examiners fingers or any object held above

the bed within his reach.

Figs. 6D(vii).2A and B: Demonstration of toe finger test.

Figs. 6D(vii).3A to E: Showing demonstration of nose finger nose test.

Nose-finger-nose test [Figs. 6D(vii).3A to E] in which the patient is asked to alternately touch their

nose and the examiner’s finger as quickly as possible. Abnormality of this is called as dysmetria.

FINGER NOSE TEST [FIGS. 6D(VII).4A AND B]

Figs. 6D(vii).4A and B: Demonstration of finger nose test.

Rebound Phenomenon [Fig. 6D(vii).5]

Fig. 6D(vii).5: Demonstration of rebound phenomenon.

DYSDIADOKOKINESIA [FIGS. 6D(VII).6A TO D]

Figs. 6D(vii).6A to D: Demonstration of dysdiadochokinesia.

FOOT TAPPING/FOOT PAT TEST [FIGS. 6D(VII).7A TO C)]

Patient is made to sit on chair with feet touching the floor flat. He is asked to pat the floor with his

forefoot. The rate, rhythm and speed of patting is compared on both sides. Even minimum cerebellar

disease can be picked up by this test.

Figs. 6D(vii).7A to C: Demonstration of foot tapping.

STRAIGHT LINE WALKING [FIGS. 6D(VII).8A AND B]

Figs. 6D(vii).8A and B: Straight line walking.

TANDEM WALKING [FIGS.6D(VII).9A AND B]

Figs. 6D(vii).9A and B: Demonstration of tandem walking.

ROMBERG TEST [FIGS. 6D(VII).10A AND B]

Patient stands still with their heels together. Ask the patient to remain still and close their eyes. If the

patient loses their balance immediately, the test is positive.

To achieve balance, a person requires 2 out of the following 3 inputs to the cortex: 1. Visual

confirmation of position, 2. Nonvisual confirmation of position (including proprioceptive and vestibular

input), and 3. A normally functioning cerebellum.

Therefore, if a patient loses their balance after standing still with their eyes closed, and is able to

maintain balance with their eyes open, then there is likely to be lesion in sensory input.

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Figs. 6D(vii).10A and B: Demonstration of Romberg’s sign.

APPROACH TO ATAXIA

Ataxia, defined as impaired coordination of voluntary muscle movement affecting the rate, range,

direction and force of movements.

It is a physical finding, not a disease.

Types of ataxia:

Cerebellar

Sensory

Vestibular

Optic

Frontal

Type of ataxia Cerebellar Sensory Frontal

Stance and support Wide based Narrow based; looking down Wide based

Velocity Variable Slow Very slow

Stride Irregular, lurching Regular with path deviation Short, shuffling

Romberg +/- Unsteady; patient falls +/-

Heel-shin Abnormal +/- Normal

Initiation Normal Normal Hesitant

Postural instability + +++ +++++

Falls Late event Frequent Frequent

Turns Unsteady +/- Multistepped; hesitant

Sensory ataxia is due to a severe sensory neuropathy, ganglionopathy or lesions of the posterior

column of the spinal cord, e.g. Sjogren’s syndrome, cisplatin, chronic inflammatory demyelinating

polyradiculoneuropathy (CIDP), paraneoplastic disorders, subacute combined degeneration (SACD),

tabes dorsalis, Miller Fischer syndrome, celiac disease.

Ataxia more at night or while walking through narrow passages (coffee plantations).

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