1. The neurological history and examination are the most important parts of the evaluation. The history should be comprehensive and determine the progression of symptoms over time. 2. The examination includes assessing mental status, cranial nerves, motor function, reflexes, sensation, coordination and gait. Abnormalities in these areas can provide clues to the underlying neurological condition. 3. Key aspects of the history include the present illness, past medical history, drug history, family history, and social history to identify risk factors and hereditary conditions.

1. Neurologic evaluation
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2. INTRODUCTION
• The history is the most important part of the neurological evaluation
• It is the history that is paramount, so it is even more important for this
to be comprehensive than the examination.
• The history and examination is critical in order to request appropriate
investigations.

3. The neurological history
• Age, sex, handedness, occupation
• History of present complaint- Start with an open question
- Determine the progression or regression of each symptom
- Determine the time course of the illness.
• Abrupt onset sensory or motor symptoms followed by improvement with variable degrees
of recovery is characteristic:- vascular events / trauma.
• Symptoms evolving over a few days, reaching a plateau in severity and then slowly
receding typically:- inflammatory CNS demyelination / multiple sclerosis.
• Subacute (developing over weeks to months), progressive symptoms:- neoplasia.

4. • Degenerative diseases have a gradual onset and a variable rate of
progression
• Tumors have a gradual onset and steady progression of symptoms, with the
rate of progression depending on the tumor type.
• Multiple sclerosis is most often characterized by remissions and
exacerbations, with a progressive increase in the severity of symptoms.
• The most frequent symptom leading to neurological referral is headache.
• Focal weakness is self-explanatory.
• The 3 most common causes of attacks of reduced consciousness or
awareness:-
- Neuro cardiogenic syncope,
- Epilepsy and
- Psychogenic non-epileptic attacks.

5. • Vertigo (a hallucination of movement);- a spinning feeling/dizziness or
giddiness/lightheadedness, loss of balance > postural hypotension or
ataxia.?. It indicates a disorder of one or both labyrinths, vestibular
nerves, vestibular nuclei in the brainstem or, rarely, the cerebrum
• Sensory symptoms may be negative (a reduction or absence of normal
sensation) or positive (an abnormal sensation which is felt:- buzzing,
tingling, ‘pins and needles’, pain).
• Neurological examination is poor at identifying and characterizing
disorders of the autonomic nervous system.
• Patients with unilateral or bilateral quadriceps weakness may present
with falls rather than complain of weakness

8. Past history
• Hypertension, diabetes, a history of previous cancer surgery in patients.
• Chronic and past illnesses; hospitalizations; accidents or injuries, particularly head trauma;
• A history of valvular heart disease or recent MI may be relevant in the patient with
cerebrovascular disease.
• A history of the patient’s birth and early development, school performance.
Drug history
• It is essential to check what prescribed drugs and OTC medicines are being taken.
• Adherence and Drugs can also cause neurological problems.
Toxin exposure
• personal habits is important, with special reference to the use of alcohol (CAGE
questionnaire ), tobacco.
Family history $ Social history
• Many neurological problems have a genetic basis so a detailed family history is often very
important in making the diagnosis.
• diabetes, hypertension, and cardiovascular disease, migraine, epilepsy, cerebrovascular
disease, movement disorders, myopathy, and cerebellar disease.

9. General Neurologic examination
Aspects of neurological examination can
start from the moment the patient is first
encountered, before and during the taking of
the history.
May yield important clues as to the
diagnosis of neurological disease.
Examination may find systemic disease with
neurological complications.

10. General appearance
• May reveal evidence of acute or chronic illness;
• Abnormal posture of the trunk, head, or extremities;
Vital signs
• RR, BP in arms , OH
• Pulse – rhythm,
HEENT
• Racoon eyes, tenderness of the superficial temporal arteries, Gross facial abnormalities.
• Kayser-Fleischer rings, exophthalmos, Perforation of the nasal septum, Notched teeth
Respiratory
• Note the respiratory rate, rhythm, depth, and character of respirations.
• Cheyne-Stokes, Kussmaul breathing
The cardiovascular examination
• Hypertension, atherosclerosis, endocarditis, arrhythmias, and valvular disease.

11. ABDOMEN
• masses, enlarged viscera, abnormal pulsations or respiratory movements, or the presence of fluid.
• Hepatomegaly, splenomegaly, Ascites
SPINE
• Note any deformity, abnormality of posture or motility, localized tenderness, or muscle spasm.
• Kyphosis (gibbus); muscular dystrophy often results in an increased lumbar lordosis; and scoliosis
is common in syringomyelia .
• Hairy patch over the lower back ,Tenderness to percussion over the spinous processes,
Skin
• Spider angiomas , purpura and petechiae, livedo reticularis, hyperpigmentation.
• Herpes zoster vesicular eruption in the distribution of the involved root.
• Peripheral nerve disease, tabes dorsalis, and myelopathy may produce trophic changes in the skin.

12. General Neurologic examination
Mental status examination
Cranial nerve examination
Motor examination
Reflex examination
Sensory examination
Coordination and Gait examination
Special examinations

13. I. Mental status examination
Mini-mental status
Orientation
Attention and concentration
Speech and Language
Memory and mood/Behaviour:
Insight and judgment
Calculation ability
Abstract thought and constructional task.

14. Level of consciousness:-
• Is alertness or state of awareness of the environment
• Consciousness depends on the interaction b/n intact cerebral hemispheres and an
important structure in the diencephalon and upper brainstem, the reticular activating
(arousal) system.
• Conscious:- fully alert having a clear sensorium
• Lethargic:- drowsy but open their eyes and look at you, respond to questions, and
then fall asleep.
• Obtunded:- Open their eyes and look at you, but respond slowly and are somewhat
confused.
• Stupor:- Only vigorous and repeated stimuli will arouse the individual and when left
undisturbed, the patient will immediately lapse back to the unresponsive
• Comatose:- patient can not be aroused

15. Assessing Glasgow Coma Scale
• Eye opening
• Verbal responsiveness
• Motor responsiveness
15

16. Mini-mental Examination = MME
• Is a standardized screening examination of cognitive function that’s
easy to administer
• Enables making the diagnosis of dementia moderate or severe to
using age-adjusted values for defining normal performance (~85%
sensitivity and specificity).
• Minimum normal performance depends on age and educational
level.
• It should not be used as more than a screening instrument for
diagnosis.

18. The Folstein mini-mental status examination (MMSE)

19. • ORIENTATION
Time—the time of day, day of the week, month, season, date and year, duration of hospitalization.
Place—the patient’s residence, the names of the hospital, city, and state.
Person—the patient’s own name, and the names of relatives and professional personnel.
With disorienting illness, time is first to be affected followed by place
• MEMORY
• Immediate/working Memory:- digit span, repeat list 3 items immediately. such as
orange, umbrella & automobile.
• Short-term/recent Memory:- recall the same three items 5 -10 min later.
• Long-term/remote memory:- Determining how well the patient is able to provide a
coherent chronologic history of his or her illness or personal events, naming presidents
in reverse order or asking historical events.
• Episodic memory;- refers to the system involved in remembering particular episodes
or experiences

20. LANGUAGE
• Fluency:- rate, flow, and melody of speech
• Content and use of words.
• Word Comprehension:- Ask the patient to follow a one-stage command or a two-
stage command. (“show me your teeth,” “close your eyes”.
• Repetition:- Ask the patient to repeat a phrase of one-syllable words (the most
difficult repetition task): “No ifs, ands, or buts.”
• Naming:- Ask the patient to name different objects.
• Reading Comprehension:- Ask the patient to follow a written command.
• Writing:- Ask the patient to write a sentence.

22. SPEECH
Rate of speech
Rhythm
Articulation
Prosody
• Abnormalities of speech need to be considered first as these may
interfere with history-taking and subsequent ability to assess higher
function and perform the rest of the examination.
• The accuracy of pronunciation, rate of speech, resonance, and
prosody (variations in pitch, rhythm, and stress of pronunciation)
are noted.

23. • INSIGHT AND JUDGMENT
Insight : perception or understanding of a situation
Judgment:- ability to assess situations accurately and form valuable opinion, decision or
conclusions.
Calculation ability
perform computations that are appropriate to the patient’s age and education.
Dyscalculia is characteristic of lesions of the dominant parietal lobe,
A commonly used calculation task is subtracting serial 7s from 100 (failing that,
serial 3s). This function also requires attention and concentration. Counting to 20
is more of a remote memory test and counting backward from 20 more of an
attentional task
Mood/Behaviour:
• Apathy; Inappropriate Euphoria; Depression
• Mood changes / fluctuations
• Temperament: Stable; Labile;

24. ABSTRACT THINKING:
Similarities b/n various objects or concepts (e.g., apple and orange, desk and
chair, poetry and sculpture) or
List items having the same attributes (e.g., a list of four-legged animals).
Interpret Proverbs =Don’t cry over spilt milk
find analogies, “table is to leg as car is to what?”
Impaired abstraction occurs in many conditions, but is particularly common
with frontal lobe disorders
Constructional task;- The task here is to copy figures of increasing
complexity.

25. II. CRANIAL NERVE EXAMINATION
The olfactory (I) nerves
• Sensory nerve :- smell
• Ensure that the nasal passages are open.
• Examine each nostril separately while occluding the other and with the
patient's eyes closed.
• Bring the test substance near the open one.
• Ask the patient to sniff and indicate whether she smells something
and, if so, to identify it.
• Repeat for the other nostril and compare the two sides.
• Use nonirritating stimuli.

26. • Because it indicates continuity of the olfactory pathways
identification of the odor indicates intact cortical function
• Perception of odor is more important than accurate Identification.
• Olfaction is the only sensation not directly processed in the thalamus.
Unilateral vs. bilateral
Conductive deficits:- due to processes interfering with the ability of
odorants to contact the olfactory epithelium.
Sensorineural or neurogenic deficits:- due to dysfunction of the
receptors or their central connections.
The top 4 causes of anosmia are URI, trauma, nasal and sinus disease
and idiopathic

27. • A person should normally perceive odor on each side, and can often
identify it.
• Loss of smell has many causes, including
- Nasal disease - Head trauma,
- Smoking, - Aging, and
- The use of cocaine - It may be congenital.
• Subfrontal tumour:- uni/bilateral anosmia
• Cribriform & plate head injury:- permanent bilateral anosmia
• Anosmia:- Lewy body disease-parkinsonism, Kallman’s syndrome.

28. Congenital or Acquired.
Neurologic origin
Meningiomas of the sphenoidal ridge
or olfactory groove and gliomas of
the frontal lobe
Head trauma- damage to the
olfactory nerves at the cribriform
plate.
Parkinson’s disease and degenerative
dementias
Multiple sclerosis
Anosmia No sense of smell
Hyposmia A decrease in the sense of
smell
Hyperosmia An overly acute sense of smell
Dysosmia Impairment or defect in the
sense of smell
Parosmia Perversion or distortion of
smell
Phantosmia Perception of an odor that is
not real

29. The optic (II) nerves
Examine cranial nerve II in the following order:
• Visual acuity with glasses on
• Visual fields
• Pupillary response
• Funduscopic exam
Visual acuity
Rough test = reading a book
Formal = Snellen’s chart (6m), Rosenbaum pocket visual screener (14 inches).
If visual acuity is <6/60 further tests with:-
o Counting fingers
o Hand movements or
o Perception of light

30. Visual fields
Confrontation test
Perimetry: used to map out visual field defects fully
or to search for subtle abnormalities.
Color vision= Using Ishihara chart
• In a stroke patient, for example—screening
indicates a visual field defect, such as a
homonymous hemianopsia
• Cranial Nerves II & III
• Inspect the size and shape of the pupils, and
compare one side with the other.
• Test the pupillary reactions to light; if these are
abnormal, examine the near response also.
• Normal size of pupil = 2-5 mm

32. • 1: Optic nerve lesion = anopsia
• 2: Optic chiasm lesion = bitemporal/heteronymous hemianopia
• 3a or 3b: Uniocular nasal hemianopia (rare).
• 3a plus 3b: Binasal hemianopia (very rare).
• 4: Optic tract lesion (incongruous homonymous hemianopia).
• 5: Visual radiation (homonymous quadrantanopia or hemianopia).
• 6a: Occipital cortex lesion sparing the occipital pole (homonymous
hemianopia with macular sparing).
• 6b: Occipital pole lesion (homonymous paracentral hemiscotoma).
• 7: A bilateral occipital cortex lesion (homonymous altitudinal
hemianopia).

33. Pupillary examination
• Use a bright torch, Size: 2-5 mm, Shape, reactions of the pupils to light/
anisocoria.
• Symmetry
• Pupillary light reflex: direct and consensual response.
• Argyll Robertson pupils: these are small, irregular, unequal pupils which do not
react to light but do to accommodation.`
 Accommodation reflex (constriction of the pupils when focusing on a near object).
• Advance your finger to a distance of about 20 cm from the patient’s face.
• Observe the adduction of the eyes and the constriction of the pupils.

34.  Optic fundi should be examined
with an ophthalmoscope
Color, size, and degree of swelling or
elevation of the optic disc, color and
texture of the retina.
 Retinal vessels size, regularity, arterial-
venous nicking at crossing points,
hemorrhage, exudates.

35. OCCULOMOTOR (CN-III), TROCHLEAR (CN-IV) AND ABDUCENS (CN-VI)
• Abnormalities of eye movements may result from disorders of the;-
- Cerebral hemispheres, - Brainstem,
- Cerebellum, - Cranial nerves III, IV and VI,
- Neuromuscular junctions b/n oculomotor nerves and eye muscles,
- Eye muscles themselves and
- Lesions affecting the structure and contents of the orbits.
• Extraocular movements:- ask the patient tracking the movement of the tip
of your finger.
• Test the extraocular movements in the 6 cardinal directions of gaze, and look
for loss of conjugate movements in any of the six directions.

36. • Identify any nystagmus (Involuntary rhythmic oscillation of one or
both eyes. )
• Look for ptosis (drooping of the upper eyelids).
• Ptosis occurs in:-
- 3rd nerve palsy,
- Horner’s syndrome (ptosis, meiosis, anhidrosis),
- Myasthenia gravis
• A slight difference in the width of the palpebral fissures may be noted
in about one third of all normal people.
• Anhidrosis = an abnormal diminution in the secretion of sweat.
• Meiosis = constriction of pupil

38. • Action of the EOMs:
- SR = Elevator - IR = Depressor
- MR = Adductor - LR = Abductor
- SO = Intorter - IO = Extorter
• Function:- The extraocular muscle cause the eyes to move together, so
that both eyes fix on the same object at the same time and binocular
(2 eyes) image is perceived by the brain.
• Oculomotor nerve (CN-III) supplies:- SR, IR, MR & IO muscles
• Trochlear nerve (CN-IV) supplies:- superior oblique muscle
• Abducent nerve (CN-VI) suppies:- lateral rectus muscle

39. The trigeminal nerve (CN V)
• This is a mixed motor and sensory nerve.
• They supply the muscles of mastication: masseter, temporalis and the
lateral pterygoids.
• Motor: While palpating the temporal & masseter muscles in turn, ask
the patient to clench ( to squeeze/hold tightly ) his or her teeth.
• Note the strength of muscle contraction.
• Weak or absent contraction of the temporal and masseter muscles on one
side suggests a lesion of CN V.
• Bilateral weakness may result from peripheral or central involvement.

40. • Sensory:
• Test the forehead, cheeks, and jaw on each side for pain sensation using safety pin
or other suitable sharp objects with the patient`s eyes closed
• Ask the patient to report whether it is “sharp” or “dull” and to compare sides.
• Unilateral decrease in or loss of facial sensation suggests a lesion of CN V

41. • Then test for light touch, using a fine wisp of cotton.
• Ask the patient to respond whenever you touch the skin
• Test the corneal reflex.
• The sensory limb of this reflex is carried in CN V, the motor response in CN VII.
• Absence of blinking suggests a lesion of CN V.
• A lesion of CN VII (the nerve to the muscles that close the eyes) may also impair this
reflex.
• The presence of a normal corneal reflex does not mean that there is no lesion of the
trigeminal nerve or its connections.

42. The facial (VII) nerve
• The facial nerve is principally a motor nerve, but it also has a small
general somatic sensory and major gustatory sensory components, as
well as important parasympathetic functions.
• Sensory : Taste anterior two-third of the tongue
• Motor: All muscles of the face & scalp except the levator palpebrae
superioris
• Inspect the face, both at rest and during conversation with the patient.
• Note any asymmetry (e.g the nasolabial folds), and observe any tics or
other abnormal movements)

43. • Ask the patient to:
- Raise both eyebrows.( “kindib”) - Frown. ( “ginbar mequater”)
- Close both eyes tightly then test muscular strength by trying to open them.
- Show both upper and lower teeth - Smile.
- Puff out both cheeks
• A unilateral upper motor neurone lesion, will cause weakness of
the lower half of the face with sparing of the upper half of the face
• Unilateral upper motor neurone lesion (supranuclealar palsy) and
lower motor neuron lesion (infranuclealar palsy).

45. VESTIBULOCOCHLEAR NURVE (CN-VIII)
• Testing for hearing
• By the use of sounds of;-
- Fingers rubbed together
- Ticking of a watch or
- Human voice
• By the use of tuning fork (512Hz or 256Hz)
 Rinne’s and Weber tests
• Nystagmus may indicate vestibular dysfunction.

47. GLOSSOPHARYNGEAL (CN IX) & VAGUS (CN X)
• CN-9 contains the motor neurons which innervate striated muscle of the
palate, pharynx, larynx and upper esophagus.
• Listen to the patient’s voice.
• Is it hoarse or does it have a nasal quality?
• Is there difficulty in swallowing? Pharyngeal or palatal weakness
• Ask the patient to say “ah” or to yawn as you watch the movements of
the soft palate and the pharynx.
• Hoarseness in vocal cord paralysis; a nasal voice in paralysis of the
palate.

48. • The soft palate normally rises symmetrically, the uvula remains in the
midline, and each side of the posterior pharynx moves medially, like a
curtain
• Gag reflex = Stroking the pharynx on each side in turn with a tongue depressor. It
may be symmetrically diminished or absent in some normal people
• The taste of posterior third of tongue
• The palate fails to rise with a bilateral lesion of the vagus nerve.

49. • Unilateral absence of gag reflex suggests a
lesion of CN IX, perhaps CN X.
• Unilateral absence signifies a lower motor
neuron lesion.
• Like most bulbar muscles the pharynx receives
bilateral supranuclear innervation, and a
unilateral cerebral lesion does not cause
detectable weakness.

50. The accessory (XI) nerve
• The spinal accessory nerve consists of motor nerve fibers from the
cervical spinal cord.
• Shoulder shrugging;- Trapezius muscle
• Head turning;- Sternocleidmastoid muscle
• From behind, look for atrophy or fasciculations in the trapezius
muscles, and compare one side with the other
• Ask the patient to shrug both shoulders upward against your hands
• Turning the head to the opposite side
• Note the strength and contraction of the trapezius and
sternocleidomastoid muscles

51. • Weakness with atrophy and fasciculations indicates a peripheral
nerve disorder.
• When the trapezius is paralyzed,
- The shoulder droops and
- The scapula is displaced downward and laterally.

52. HYPOGLOSSAL NERVE (CN XII)
• The hypoglossal nucleus in the medulla contains
motor neurons which innervate tongue muscles.
Look at the tongue :asymmetry, atrophy, tremor and
fasciculation.
Symmetry of movement (side-to-side)
Check for strength pushing against inside cheek as you
palpate externally.
 Attempted protrusion of the tongue results in
deviation of the tongue toward the weak side.
In a unilateral cortical lesion, the protruded tongue
deviates transiently in a direction away from the side
of the cortical lesion.

53. III. MOTOR EXAMINATION
• III A. Appearance
• This requires complete exposure of limbs, shoulders, trunk and buttocks.
• Inspect:- Position: look for any deformity or lateralization sign, spontaneous muscle
fasciculation, atrophy or hypertrophy/‘pseudohypertrophy’.
 Involuntary movements at rest (e.g., tics, myoclonus), during maintained posture (pill-rolling tremor of
Parkinson’s disease).
 Voluntary movements (intention tremor of cerebellar disease or familial tremor).
• Palpate muscle groups:-
Measure the bulk and Compare both sides with tape meter.
Check for induced muscle fasciculation, tenderness, and hypertrophy.

54. • Measure in Cm from same reference. Difference of >2 cm is significant
• Muscular atrophy refers to a loss of muscle bulk (wasting). It results from
diseases of the peripheral nervous system such as diabetic neuropathy,
as well as diseases of the muscles themselves.
• Wasted muscles are softer & flabby than normal
• Hypertrophy refers to an increase in bulk with proportionate strength,
while increased bulk with diminished strength is called
pseudohypertrophy

55. III B. Muscle Tone
• When a normal muscle with an intact nerve supply is relaxed voluntarily, it
maintains a slight residual tension known as muscle tone.
• This can be assessed by feeling the muscle’s resistance to passive stretch
• Take one hand with yours and, while supporting the elbow, flex and extend
the patient’s fingers, wrist, and elbow
• On each side, note muscle tone—the resistance offered to your movements.
- Normal tone
- Hypotonia  LMNL
- Hypertonia  UMNL

56. • Tested by measuring the resistance to passive movement of a relaxed limb.
• Repeat each movement at different speeds.
Normal
Hypotonia: flaccidity suggests LMN or cerebellar lesion.
Hypertonia:
Spasticity (Clasp- knife);- resistance determined by the angle and velocity of motion. Seen in
corticospinal or UMNL.
Lead-pipe rigidity: similar resistance in all angles of motion.
Cogwheel rigidity: passive motion elicits jerky interruptions in resistance. ExP
syndrome, parkinsonism, Phenothizine.
Paratonia : fluctuating changes in resistance; Bilateral frontal lobe pathways damage or
normal difficulty in relaxing.

57. • Marked floppiness indicates hypotonic or flaccid muscles.
• Spasticity (clasp knife type) =  tone with rapidly flexed or
extended limb
• Cog wheel rigidity =  resistance throughout passive mov’
with jerky interruptions
• Lead pipe (plastic) type =  tone with uniform resistance
throughout passive mov’t  extrapyramidal tract lesion
• Paratonia - fluctuating changes in resistance - frontal lobe
lesions.

58. III C. STRENGTH
A person’s dominant side is usually slightly stronger than the other side.
Patient may place a joint in a certain position, and then the examiner tries to move it. Or the
patient may try to move a joint or contract a muscle against the fixed resistance of the
examiner.
Observation and palpation of either the contraction of the muscle belly or its movement of its
tendon may be helpful adjuncts.
UMNL  Proximal + distal weakness (monoparesis, hemiparesis, paraparesis, tetraparesis).
Proximal weakness alone  myopathy (NMJ or muscle) e.g. Myasthenia gravis/
demyelinating polyneuropathies.
Distal symmetrical weakness alone  peripheral neuropathy.
Non-organic weakness:- reflect malingering or a conversion disorder

59. III D. POWER
British Medical Research Council Grading
• 0 = no movement
• 1 = flicker or trace of contraction but no
associated movement at a joint
• 2 = movement with gravity eliminated
• 3 = movement against gravity but not against
resistance
• 4− = movement against a mild degree of
resistance
• 4 = movement against moderate resistance
• 4+ = movement against strong resistance
• 5 = full power
Paralysis = no movement
Severe weakness = movement
with gravity eliminated
Moderate weakness = movement
against gravity but not against mild
resistance
Mild weakness = movement
against moderate resistance
Full strength

60. • Impaired strength is called weakness (paresis).
• Absence of strength is called paralysis (plegia).
• Hemiparesis refers to weakness of one half of the body; hemiplegia to
paralysis of one half of the body.
• Paraplegia means paralysis of the legs;
• Quadriplegia, paralysis of all four limbs.
• Strength may be classified as;-
• Kinetic;- the force exerted in changing position, and
• Static;- the force exerted in resisting movement from a fixed position.

61. III D. COORDINATION
• Coordination of muscle movement requires that four areas of the
nervous system function in an integrated way:
• The motor system, for muscle strength
• The cerebellar system
• The vestibular system, for balance and for coordinating eye, head, and body
movements
• The sensory system, for position sense
• To assess coordination, observe the patient’s performance in:
 Rapid alternating movements
 Point-to-point movements
 Gait and other related body movements
 Standing in specified ways

62. • Rapid Alternating Movements
• ARMS
• Show the patient how to strike one hand on the thigh, raise the hand, turn it over,
and then strike the back of the hand down on the same place.
• Urge the patient to repeat these alternating movements as rapidly as possible
• Show the patient how to tap the distal joint of the thumb with the tip of the index
finger, again as rapidly as possible
• Ask the patient to touch your index finger and then his or her nose alternately
several times.
• Move your finger about so that the patient has to alter directions and extend the
arm fully to reach it
• Cerebellar disease, Upper motor neuron weakness & basal ganglia disease may
impair rapid alternating movements.
• Irregularity and clumsiness indicate an ipsilateral cerebellar hemisphere disturbance.

64. • LEGS
• Ask the patient to tap your hand as
quickly as possible with the ball of
each foot in turn
• Ask the patient to place one heel on
the opposite knee, and then run it
down the shin to the big toe (heel to
shin test)

65. • Gait;- Ask the patient to:
• Walk across the room or down the hall, then turn, and come back.
Observe posture, balance, swinging of arms, and movements of the
legs.
• Walk heel-to-toe in a straight line
• Walk on the toes, then on the heels
• Inability to heel-walk is a sensitive test for corticospinal tract
weakness.

67. • Stance = THE ROMBERG TEST
• The patient should first stand with feet together and eyes open and then
close both eyes for 20-30 seconds without support.
• Normally only minimal swaying occurs

68. Romberg’s sign
• In ataxia due to loss of position sense, vision
compensates for the sensory loss.
• The patient stands fairly well with eyes open but
loses balance when they are closed, a positive
Romberg sign.
• In cerebellar ataxia, the patient has difficulty
standing with feet together whether the eyes are
open or closed.
• Romberg’s test cannot be performed if the patient cannot stand unaided.
• Romberg’s test is not positive in cerebellar disease.
• If he falls with his eyes open you cannot proceed with the test.
• If not: Ask the patient to close his eyes

69. • PRONATOR DRIFT (Barré's sign);- The patient should stand for 20-30
seconds with both arms straight forward, palms up, and with eyes closed.
• In either case, a normal person can hold this arm position well.
• The pronation of one forearm suggests a contralateral lesion in the
corticospinal tract

70. Moderate drift
Mild drift
The patient should hold this position for at least 20 to 30 seconds.
In normals, the palms will remain flat, the elbows straight, and the limbs horizontal

71. IV. REFLEXES
• The tendon reflexes provide information about both the motor system
and the sensory system.
• The tendon reflex, cutaneous reflexes & plantar reflexes comprise the major
commonly tested reflexes.
• The tendon of the relevant muscle being tested is briskly & effectively struck.
• The DTRs usually examined include the biceps, triceps, brachioradialis, knee
(quadriceps), and ankle (Achilles) tendon reflexes.
• Reinforcement : Jendrassik maneuver
• Sudden stretching of a muscle by striking its tendon sends an impulse from muscle
spindle afferents which synapse directly with motor neurons, leading to reflex
contraction of that muscle.
• But areflexia more commonly reflects a sensory rather than a motor system
disorder.
• Normal individuals who have absent reflexes tested in the standard way will usually
have reflexes if they are brought out by reinforcement.

73. Grading reflexes
• Clonus (ankle, patellar)
- 2- 3 clonus = unsustained (physiological)
- > 3 clonus = sustained  UMNL
• Clonus = rhythmic
oscillations
between flexion
and extension

74. • Hyperactive reflexes suggest central nervous system disease. Sustained
clonus confirms it.
• Reflexes may be diminished or absent :-
- When sensation is lost,
- When the relevant spinal segments are damaged, or
- When the peripheral nerves are damaged.
• The Biceps Reflex (C5, C6) The Triceps Reflex (C6, C7)

75.  The Knee Reflex (L2, L3, L4)
• The patient may be either sitting or lying down as long as the
knee is flexed
• Briskly tap the patellar tendon just below the patella. Note
contraction of the quadriceps with extension at the knee

76.  The Ankle Reflex (primarily S1)
• If the patient is sitting, dorsiflex the foot at the ankle
• Strike the Achilles tendon. Watch and feel for plantar flexion at
the ankle.
• Note also the speed of relaxation after muscular contraction

77. • When the patient is lying down, flex one leg at both hip and knee and
rotate it externally so that the lower leg rests across the opposite shin.
• Then dorsiflex the foot at the ankle and strike the Achilles tendon

78. Cutaneous reflexes
• Superficial Abdominal Reflex
Helpful when there is preservation of the upper (spinal cord level T9) but not
lower (T12) abdominal reflexes.
• Cremasteric Reflex
Ipsilateral elevation of the testicle following stroking of the medial thigh.
Mediated by L1 & L2.
• Anal Wink Reflex
Contraction of the anal sphincter when the perianal skin is scratched
Mediated by S2-S4.

79. • The reflex is absent in spinal lesions above
the level at which the reflex is being tested
and the reflexes are sometimes absent at a
very early stage in multiple sclerosis.

80. PLANTAR REFLEX
• Hold the patient’s foot.
• Apply the orange stick to the sole of the foot on the lateral border just
in front of the heel.
• Draw it forward towards the base of the fifth toe.
• Try to do the test effectively once or twice, not a large number of times.
• Usually stopping at the MTP joints or extending medially over
metatarsal pad from the little toe/ reinforced by rotating the patient's
head to the opposite side.
• It may be inhibited when the foot is cold and increased when the foot is
warm.

81. Remarkably reliable feature of an upper motor neuron
lesion.
Plantar stimulation must be carried out far laterally, in
the S1 root/sural nerve sensory distribution.
Normal response;- flexion of toes.
Minimal response;- dorsiflexion of the great toe.
 Additionally fanning out of other toes
Marked response;- flexion knees and hips and
dorsiflexion of the ankle and fanning out of other toes.
 Spontaneous Babiniski
Babinski sign
• Dorsiflexion of the big toe, often accompanied by
fanning of the other toes, constitutes a Babinski
response.
• It often indicates a central nervous system lesion in
the corticospinal tract

82. Clonus
• If the reflexes seem hyperactive, test for ankle
clonus. Support the knee in a partly flexed position.
• With your other hand, dorsiflex and plantar flex the
foot a few times while encouraging the patient to
relax, and then sharply dorsiflex the foot and
maintain it in dorsiflexion
• Look and feel for rhythmic oscillations between
dorsiflexion and plantar flexion

83. Meningeal signs
• a) Nucheal rigidity (neck stiffness):- with the patient supine, place your
hands behind the patient’s head and flex the neck forward, until the chin touches the
chest if possible. Normally the neck is supple and the patient can easily bend the head
and neck forward.
• Pain in the neck and resistance to flexion can arise from meningeal inflammation,
arthritis, or neck injury.
• b. Kernig`s sign;- Flex the patient’s leg at both the hip and the knee, and then
straighten the knee.
• Pain and increased resistance to extending the knee are a positive Kernig’s sign. When
bilateral, it suggests meningeal irritation.
• c. Brudzinski`s sign;- As you flex the neck, watch the hips and knees in
reaction to your maneuver.
• Normally they should remain relaxed and motionless.
• Flexion of the hips and knees is a positive Brudzinski’s sign and suggests meningeal
inflammation.

84. Feature Upper Motor Neuron Lower Motor Neuron
Weakness distribution Corticospinal distribution; hemiparesis,
quadriparesis, paraparesis,
monoparesis,
Generalized, predominantly proximal,
predominantly distal or focal.
Sensory loss distribution Central pattern None, stocking glove or peripheral
nerve or root distribution
Deep tendon reflexes Increased unless very acute Normal or decreased
Superficial reflexes Decreased Normal
Pathological reflexes Yes No
Sphincter function Sometimes impaired Normal (except for cauda equina
lesion)
Muscle tone Increased Normal or decreased
Pain No Sometimes
Other CNS signs Possibly No

85. V. The Sensory System
• To evaluate the sensory system, you will test several kinds of sensation:
- Pain and temperature (spinothalamic tracts)
- Position and vibration (posterior columns)
- Touch (both of these pathways)
- Discriminative sensations, which depend on some of the above sensations but also involve
the cortex
All sensory tests are subjective –with few exceptions
Goal : To see whether any hypoaesthesia conforms to a meaningful pattern.
Defining an area of hypoaesthesia –better starting testing within the area of hypoaesthesia and moving
the stimulus out into areas where sensation is normally perceived.
Testing for primary modalities and Cortical sensation.
Light touch- dabbing with cotton wool
Pinprick
Pressure/touch –10gm monofilament- apply standard quantity
Thermal

86. Pin prick
• Ask the patient to close his eyes then apply randomly sharp and
blunt stimuli and note the patient’s response.
• Use a pin—a disposable neurological pin, or dressmaker’s or
safety pin.
Light touch
• Use a piece of cotton wool /a fingertip and Dab this on to the skin.
• Ask the patient to close his eyes; test the areas as for pin prick.
• Apply the stimulus at random intervals.
• Ask the patient to respond whenever a touch is felt, and to compare
one area with another

87. Temperature sensation
• This is often omitted if pain sensation is normal, but include
it if there is any question.
• Use two test tubes, filled with hot and cold water, or a
tuning fork heated or cooled by water.
• Touch the skin and ask the patient to identify “hot” or “cold.”
Sacral sensation: this is not usually screened, Test sacral
sensation in any patient with:
• Urinary or bowel symptoms and bilateral leg weakness
• Sensory loss in both legs.

88. Proprioception
JOINT POSITION SENSE
• Grasp the patient’s big toe, holding it by its sides between your
thumb and index finger, and then pull it away from the other toes so
as to avoid friction.
• Demonstrate “up” and “down” as you move the patient’s toe clearly
upward and downward.
• Then, with the patient’s eyes closed, ask for a response of “up” or
“down” when moving the toe in a small arc.
• Polyneuropathies, spinal cord lesions affecting the posterior columns
and in lesions at higher levels including lesions of the sensory cortex.
• Loss of position sense, like loss of vibration sense, suggests either posterior
column disease or a lesion of the peripheral nerve or root.
Romberg’s test

89. Vibration sense
o Use a 128 Hz tuning fork.
• Apply the base of the tuning fork to bony parts of the limbs and ask the patient to report
whether he feels the vibrations.
Tested with eyes closed from Distal to proximal.
• A useful sign of either a polyneuropathy or a spinal cord lesion.
• Tap the tuning fork on the heel of your hand and place it firmly over a
distal interphalangeal joint of the patient’s finger, then over the
interphalangeal joint of the big toe.
• Vibration sense is often the first sensation to be lost in a peripheral
neuropathy.
• Common causes include diabetes and alcoholism.

91. • Because discriminative sensations depend on touch and position
sense, they are useful only when these sensations are either intact or
only slightly impaired
• Symmetric distal sensory loss suggests a polyneuropathy
• Analgesia refers to absence of pain sensation, hypalgesia to
decreased sensitivity to pain, and hyperalgesia to increased
sensitivity.

92. CORTICAL SENSATION
Tested requires intact primary modalities sensation.
 Sterognosis:- to identify an object by feeling it.
Graphastesia (traced Figure Discrimination)

93. Sensory Inattention or Extinction: loss of the ability to perceive two
simultaneous sensory stimuli.
• double simultaneous light touch stimuli at homologous sites on the two sides of
the body.
Two-point/Spatial Discrimination
• Normal two-point discrimination is about 2 mm to 4 mm on the fingertips, 4
mm to 6 mm on the dorsum of the fingers, 8 mm to 12 mm on the palm, 20 mm to
30 mm on the dorsum of the hand, and 30 mm to 40 mm on the dorsum of the
foot.
• Compare both sides.
93

94. • Two-point/Spatial Discrimination;- ability to differentiate, eyes closed,
cutaneous stimulation by one point from stimulation by two points
• Normal two-point discrimination is about 1 mm on the tip of the tongue,
2 mm to 3 mm on the lips
• Tactile extinction is most likely to occur with a lesion of the parietal lobe
• Sterognosis;- perception, understanding, recognition & identification of
the form & nature of objects by touch
• Size then shape then form and finally recognition
• Graphastesia;- ability to recognize letters or numbers written on the
skin with a pencil, dull pin, or similar object.

95. UMN
• The cell bodies of UMNs are in the cerebral cortex and in the brainstem
• The axons of UMNs descend into the spinal cord in tracts to reach and
synapse directly with LMNs, or with interneurons which then synapse
with LMNs.
• In most cases, the neuronal cell bodies of UMNs are on the opposite
(contralateral) side of the midline of the CNS than the LMNs that they
innervate.
• Structures in the brainstem that contain UMNs include the red nucleus,
the pontine and medullary reticular formation, and the lateral and
medial vestibular nuclei.
10/21/2023 95

96. Lower Motor Neurons
• LMNs with cell bodies in lamina IX of the ventral horn of the spinal cord
• The cell bodies of the alpha and gamma LMNs in the spinal cord are
always on the same (ipsilateral) side of the midline of the CNS as the
skeletal muscles that their axons innervate.
10/21/2023 96

97. • Feature of UMNL depending on the site.
• Elevated or hyperactive muscle stretch reflexes (hyperreflexia or
hypertonicity);- because UMN systems have a net overall inhibitory
effect on muscle stretch and inverse muscle stretch reflexes.
• Primary motor area (A4) lesions and its fibers
• Thrombosis of lenticulostriatal artery
• Damage to the cortex itself
• Produces crossed monoplegia or contralateral facial paralysis
• Corona radiate = Crossed monoplegia/hemiplegia
97
Upper Motor Neuron Lesion (UMNL)

98. • The hyperactive muscle stretch reflexes seen in patients with UMN
lesions is mainly due to a loss of inhibition of gamma motor neurons by
reticulospinal medullary UMNs.
• Patients with hyperactive muscle stretch reflexes may have clonus, which
is characterized by rapid successive reflex contractions and relaxations
of agonists and antagonists observed mainly at the knee and ankle joints
during reflex testing.
10/21/2023 98

99. • A clasp knife reaction is an indication of a loss of upper motor inhibition
of the inverse muscle stretch reflex
• In a clasp knife reaction, stretching of a hypertonic contracted muscle
abnormally increases muscle force and thereby increasing the activity of
Golgi tendon organ (GTOs).
• The increased activity in GTOs results in a sudden release of resistance
when the muscle is stretched and a relaxation of the hypertonic muscle.
10/21/2023 99

100. 10/21/2023 100
• Altered cutaneous reflexes;- The Babinski sign is the best- known
example of an altered cutaneous reflex.
• Normally, the toes flex in response to a plantar cutaneous stimulus.
Patients with a UMN lesion may have a Babinski sign, characterized by
an extensor plantar response (extension of the great toe and fanning of
the other toes).
• A Babinski sign is normal in infants until the UMN tracts become
fully myelinated.

101. Babiniski sign
• Cutaneous reflex
• UMNL produces this reflex
a. Normal plantar flexion
b. Dorsiflexion of big toe and
fanning of the other toes
normal in infants
101

102. 10/21/2023 102
• Two other cutaneous reflexes —the abdominal reflex, which uses
the T8 through T12 spinal segments, and cremasteric reflex,
which uses the L1 spinal segment —are paradoxically absent in
patients with UMN lesions
• In a normal abdominal reflex, stroking the skin of the abdomen
results in reflex contraction of abdominal wall muscles with
movement of the umbilicus toward the stimulus.

103. 10/21/2023 103
• Atrophy of weakened muscles;- result of disuse but contract by stimulating
muscle stretch reflexes.
• Lesions of UMNs result in a spastic paresis that may be ipsilateral or
contralateral to the lesion and is always below the lesion.
• A lesion of axons of UMNs in the spinal cord results in a spastic paresis that is
ipsilateral and below the level of the lesion.
• A lesion of UMNs between the cerebral cortex and the medulla above the
decussation of the pyramids will result in a spastic paresis that is contralateral
and below the level of the lesion.

104. • Lession in internal capsule
• Crossed hemiplegia (paralysis of half part)
• Crossed Hemianesthesia (reduced sensations)
• Homonimous hemianopia (loss of corresponding half of the
visual field)
• Bilateral diminished hearing
• Decorticate rigidity (thalamic response)
• A sign of removal of cerebral cortex with a loss of fine sensations,
appearance of rage (hypothalamic dominance)
• Increased muscle tone in antigravity muscles causing limb extensions with
upper hand flexion
• Due to withdrawal of inhibitory input to Vestibular and Reticular nuclei
104

105. • Lesion at brain stem
• Midbrain: Crossed hemiplegia + ipsilateral diplopia (ocular muscle
paralysis result in reduced conjugate eye movement: III, IV)
• Decerebrate rigidity
Results from sectioning across the mid brain
Characterized by loss of sensation and temp. control
Tonic contraction of antigravity muscles with head and limb
extentions
It results from release of vestibular and reticular formation
from cortical inhibitions
105

106. •Lower Motor Neuron Lesion
• Failure of spinal centers below the damage with flaccid paralysis
(withdrawal of facilitatory higher centers) resulting in spinal shock
(2-4 wk)
• Loss of all sensations: cutaneous, deep, visceral
• Loss of superficial deep and visceral reflexes
• Flaccid paralysis of skeletal muscles and loss of muscle tone
• Loss of vasomotor tone (vasodilatation and hypotension)
106

107. UMN AND LMN lesion
Criteria UMNL LMNL
Cause Pyramidal tract lesion Anterior horn lesion
Paralysis
Type
Extent
Spastic
Widespread
Flaccid
Localized
Reflexes
Cutaneous
Babniski sign
Deep reflex
Lost
Present
Exaggerated
Lost
Absent
Absent
Muscle tone/wasting Increased/Minimal Decreased/ Marked
Response to electric
stimulation
Normal Reaction of degeneration
(10-14 days after)
107