Fig. 6D(x).5: Brudzinski’s leg sign/reflex.
Fig. 6D(x).6: Illustration of Brudzinski’s sign.
Fig. 6D(x).8: Tripod sign (Amoss’s sign).
Tripod sign, also known as the “Amoss’s sign”, is a useful sign of meningeal irritation.
The patient is asked to sit up in bed. This action requires active movement involving flexion of the
neck. Although a normal patient sits up without supporting himself, a patient with meningeal irritation
tries to sit up by supporting himself with his hands placed far behind him in the bed (like a tripod), in
order to take the weight off the spine and prevent its flexion [Fig. 6D(x).8]. Severe meningeal irritation
may result in the patient assuming the tripod position with the knees and hips flexed, the back arched
lordotically, the neck extended, and the arms brought back in a plane posterior to the pelvis to support
the thorax.
MENINGISM
Meningism, also called meningismus or pseudomeningitis, is a set of symptoms similar to those of
meningitis but not caused by meningitis. Whereas meningitis is inflammation of the meninges
(membranes that cover the central nervous system), meningism is caused by nonmeningitic irritation of
the meninges usually associated with acute febrile illness, especially in children and adolescents.
Causes
Meningism:
Meningitis
Subarachnoid hemorrhage.
Other conditions that mimic meningism (also resist cervical rotation):
Cervical spondylosis
After cervical fusion
Parkinson’s disease
Raised intracranial pressure especially if there is impending tonsillar herniation
Acute dystonic reaction
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Tetanus
Strychnine poisoning.
Intermittent neck stiffness is characteristic of Arnold-Chiari malformation.
EXAMINATION OF SKULL
Size of skull—microcephaly, macrocephaly
Shape/deformities
Tenderness—fracture/metastasis
Crackpot sound on percussion—hydrocephalus
Bruits on auscultation—arteriovenous malformation (AVM), hemangioma.
EXAMINATION OF SPINE
Inspection—deformities, curvature—kyphosis, scoliosis, lordosis, dimple, tuft of hair, Pott’s spine, and
meningioma
Palpation—tenderness, paraspinal spasm, and deformities
Movements [Figs. 6D(x).9A and B].
Figs. 6D(x).9A and B: Movements of spine. (Details discussed under rheumatology section)
AUTONOMIC NERVOUS SYSTEM TESTING
Common autonomic
symptoms
Signs
Orthostatic
intolerance
Dizziness
Lightheadedness
Fatigue
Pupils—mid-dilated sluggish reacting pupil
Pedal edema
Resting tachycardia
Postural hypotension
Palpable urinary bladder
Sweating abnormalities
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“Coat hanger”
headache
Nausea
Palpitations
Near syncope and
syncope
Genitourinary
Bladder urgency or
frequency
Incontinence
Nocturia
Erectile dysfunction
Ejaculatory
disturbances
Common autonomic
symptoms
Signs
Gastrointestinal
Diarrhea
Constipation
Fecal incontinence
Postprandial
fullness, cramping,
or bloating
Sudomotor
Hyperhidrosis
Hypohidrosis and
anhidrosis
Tests
Cardiovagal
innervation
(parasympathetic
innervation)
Heart rate (HR)
response to deep
breathing
Valsalva ratio, and
HR response to
standing (30:15
ratio)
“Spoon test”: A kitchen soup spoon, with its curved surface resting on the skin, was held between the
thumb and forefinger, and was drawn slowly on the skin, using sufficient energy to overcome its weight
without lifting it from the skin. When “sympathectomized” skin was crossed, the pull was smooth and
unopposed; but where sweat gland innervation and sympathetic function was intact, the skin was moist,
and the flow of the spoon was interrupted, and became sticky requiring readjustment of the strength of
pull
Adrenergic
Beat-to-beat blood
pressure (BP)
responses to the
Valsalva maneuver,
sustained
handgrip/diastolic
hand grip test ** and
BP and HR
responses to tilt-up
or active standing
“Sustained handgrip test (SHT): This parameter indicates cardiac sympathetic response and DBP
response to the sustained handgrip test—taken as the difference between the DBP just before release
of handgrip and the mean of three resting DBP readings. The change in mean DBP in response to
sustained handgrip test was interpreted as:
≥16 mm Hg was taken as normal
11–15 mm Hg as borderline
≤10 mm Hg as abnormal
Sudomotor:
Quantitative
sudomotor axon
reflex test (QSART)
Thermoregulatory
sweat test (TST)
Sympathetic skin
response (SSR),
and
Silastic sweat imprint
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Head-Up Tilt-Table Testing
The patient lies supine on the tilt table. Beat-to-beat and oscillometric BP instruments are attached to
each arm. ECG monitoring should take place throughout the test. Once the patient is comfortable, with
feet resting on the footboard, a baseline BP is recorded for at least 3 minutes. The patient is then slowly
tilted upright to an angle of 60–80°.
During testing, the patient is asked to report any symptoms. Both BP and HR are recorded
throughout tilt-table testing, after which the patient is returned to a horizontal supine position.
Three well-described patterns of neurally-mediated syncope can occur during head-up tilt-table
testing:
Vasodepression resulting in hypotension without bradycardia.
Cardioinhibition with a marked bradycardia (fewer than 40 beats/min) with or without significant
hypotension.
Mixed, with both bradycardia and hypotension.
Valsalva Ratio
The Valsalva maneuver consists of respiratory strain which increases intrathoracic and intra-abdominal
pressures and alters hemodynamic and cardiac functions.
The patient is supine or with head slightly elevated to about 30°.
Have the patient strain against 40 mm Hg applied for 15 seconds by blowing into a mouthpiece
attached to a sphygmomanometer.
Following cessation of the Valsalva strain, the patient relaxes and breathes at a normal comfortable
rate.
The ECG is monitored during the strain and 30–45 seconds following its release.
The maximal heart rate of phase II actually occurs about 1 seconds following cessation of the strain.
The minimal heart rate occurs about 15–20 seconds after releasing the strain.
DISEASES ASSOCIATED WITH AUTONOMIC DYSFUNCTION [TABLE
6D(X).1]
Table 6D(x).1: Diseases commonly associated with autonomic dysfunction.
Preganglionic autonomic failure:
Multiple system atrophy
Parkinson’s disease with autonomic failure
Ganglionic and postganglionic disorders
Pure autonomic failure
Peripheral neuropathies and neuronopathies with autonomic dysfunction
Acute and subacute (preganglionic and postganglionic):
Acute pandysautonomia
Guillain-Barré syndrome
Paraneoplastic pandysautonomia
Others (porphyria, toxins, durgs)
Chronic small-fiber (postganglionic) neruopathies:
Diabetes
Amyloidosis
Hereditary (familial dysautonomia, Fabry’s disease)
Subacute or chronic sensory and autonomic ganglionopathies:
Paraneoplastic
Sjogren’s syndrome
Other peripheral neuropathies:
Infections (human immunodeficiency virus)
Connective tissue disease (systemic lupus erythematosus)
Metabolic-nutritional (alcohol, uremia, vitamin B12 deficiency)
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4.
E. A PPROACH TO COMMON NEUROLOGICAL CASES
Approach to following cases have been discussed in this section:
Approach to cerebrovascular accident
Approach to spinal cord diseases
Approach to neuropathy
Approach to movement disorders
Flowchart 6E.1: Diseases stratification of nervous system.
(UMN: upper motor neuron; LMN: lower motor neuron; CVA: cerebrovascular accident; TIA: transient
ischemic attack; CVST: cerebral venous sinus thrombosis; SAH: subarachnoid hemorrhage; TBM:
tuberculous meningitis; HSV: herpes simplex virus; PML: promyelocytic leukemia; SACD: subacute
combined degeneration; AIDP: acute inflammatory demyelinating polyneuropathy; CIDP: chronic
inflammatory demyelinating polyneuropathy; NMJ: neuromuscular junction)
1. APPROACH TO CEREBROVASCULAR ACCIDENT
Table 6E.1: Signs of upper and lower motor neuron disease.
Sign Upper motor neuron Lower motor neuron
Atrophy None (rarely disuse atrophy) Severe wasting
Fasciculations None Common
Tone Hypertonia—rigidity/spasticity Decreased (hypotonia)
Distribution of weakness Distal predominant/regional Predominantly proximal (except neuropathy)/segmental
Tendon reflexes Exaggerated/hyperactive Hypoactive/lost
Babinski sign Present Absent
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