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A Dictionary of Neurological Signs

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Weakness

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trunk movements, but in rigidity the limbs and trunk tend to move en bloc. Passive swinging of the wrist or elbow joint may also be performed to assess rigidity.

Cross References

Parkinsonism; Rigidity; “Rolex” sign; Spasticity

Wasting

Wasting refers to a thinning of the musculature, also known as atrophy or, if of neurogenic origin, amyotrophy.

Wasting may be a consequence of disorders of:

Muscle (myopathies, dystrophies)

Peripheral nerve (more so in axonal than demyelinating peripheral neuropathies)

Anterior horn cells (e.g., motor neurone disease).

Wasting may occur in chronic upper motor neurone syndromes (e.g., chronic hemiplegia) but is not as evident as in lower motor neurone syndromes where wasting may appear subacutely (over a few weeks).

Wasting may also be seen in general medical disorders associated with a profound catabolic state, e.g., cancer cachexia, uncontrolled heart failure, liver cirrhosis, renal failure.

Cross References

Amyotrophy; Atrophy; Lower motor neurone (LMN) syndrome; Upper motor neurone (UMN) syndrome

Weakness

Weakness is an objective loss of muscle strength. This is conveniently quantified or rated using the MRC grading system:

5 = normal power

4 = active movement against gravity and resistance

3 = active movement against gravity

2 = active movement with gravity eliminated

1 = flicker or trace of contraction

0 = no contraction (paralysis).

However, this is not a linear scale; grade 4 often becomes subdivided into 4−, 4, and 4+ (or even 5−) according to the increasing degree of resistance which the examiner must apply to overcome activity. It is also important to assess what effort the patient is making to comply with the testing; “apparent weakness” or “pseudoparesis” may be shorthand for lack of patient effort. Sudden “giving way” of muscle contraction may be an indicator of this. Nonuniform resistance may also be due to pain (algesic pseudoparesis). Testing records only the best forced maximal contraction, and should not develop into an unseemly trial of strength between patient and examiner. Accepting all these difficulties, it should be acknowledged that the grading of weakness, like all clinical observations, is subject to some degree of observer bias.

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Weber’s Test

The pattern of muscle weakness may suggest its anatomical origin. So-called “pyramidal weakness” (i.e., affecting upper limb extensors more than flexors, and lower limb flexors more than extensors), suggests an upper motor neurone lesion (corticospinal pathways). However, there is no evidence that pure lesions of the pyramidal tracts produce this picture: pyramidotomy in the monkey results in a deficit in fine finger movements, but without weakness. Moreover, a similar pattern of weakness may be observed in lower motor neurone disorders, such as Guillain-Barré syndrome. Coexistent wasting suggests muscle weakness is of lower motor neurone origin, especially if acute, although wasting may occur in long-standing upper motor neurone lesions. Weakness with minimal or no muscle wasting may be nonorganic, but may be seen in conditions, such as multifocal motor neuropathy with conduction block.

References

Aids to the Examination of the Peripheral Nervous System. London: HMSO, 1976

Cross References

Collapsing weakness; Hyperreflexia; Lower motor neurone (LMN) syndrome; Upper motor neurone (UMN) syndrome; Wasting

Weber’s Test

Weber’s test is one of the tuning fork tests, which may be used to confirm a conductive component in unilateral or asymmetric hearing loss. The vibrating tuning fork is put on the middle of the forehead and the patient asked in which ear it is heard; this depends entirely upon bone conduction (BC). Hence the sound localizes to the side of a conductive hearing loss (where bone conduction is greater than air conduction, BC > AC), and away from the side of a sensorineural hearing loss.

References

Miyamoto RT, Wynne MK. Approach to the patient with hearing loss. In: Biller J (ed.). Practical neurology (2nd edition). Philadelphia: Lippincott Williams & Wilkins, 2002: 206-226

Cross References

Rinne’s test

Wernicke’s Aphasia

Wernicke’s aphasia is the classical “receptive aphasia,” in distinction to the “expressive aphasia” of Broca, although this classification is problematic since there are concurrent “expressive” problems in Wernicke’s aphasia.

Considering each of the features suggested for the clinical classification of aphasias (see Aphasia), Wernicke’s aphasia is characterized by:

Fluency: fluent speech with phonemic and semantic paraphasias and paragrammatism (inappropriate use of syntax); “empty speech” with few verbs and nouns; prosody usually preserved; at worst, flowing speech (logorrhea) devoid of semantic meaning (jargon aphasia, semantic aphasia); automatic speech is often bet-

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Wheelchair Sign

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ter preserved than spontaneous, e.g., counting, days of week, overlearned phrases (“I’m fine”).

Comprehension: impaired auditory comprehension (sine qua non; “word deafness”); impaired reading comprehension probably also required (not specifically discussed by Wernicke).

Repetition: impaired.

Naming: severely impaired (anomia) and not aided by cueing (cf. Broca’s aphasia).

Reading: usually impaired, with numerous paralexic errors, and impaired reading comprehension (cf. pure word deafness).

Writing: similarly affected.

There may be associated anxiety, with or without agitation and paranoia, and concurrent auditory agnosia.

The neuroanatomical substrate of Wernicke’s aphasia has been a subject of debate. Wernicke placed it in the posterior two-thirds of the superior temporal gyrus and planum temporale (Brodmann area 22), but more recent neuroradiological studies (structural and functional imaging) suggest that this area may be more associated with the generation of paraphasia whereas more ventral areas of temporal lobe and angular gyrus (Brodmann areas 37, 39 and 40) may be associated with disturbance of comprehension. A correlation exists between the size of the lesion and the extent of the aphasia. A similar clinical picture may occur with infarcts of the head of the left caudate nucleus and left thalamic nuclei.

The differential diagnosis of Wernicke’s aphasia includes delirium and schizophasia.

References

Binder JR. Wernicke aphasia: a disorder of central language processing. . In: D’Esposito M (ed.). Neurological foundations of cognitive neuroscience. Cambridge: MIT Press, 2003: 175-238

Wise RJS, Scott SK, Blank SC, Mummery CJ, Murphy K, Warburton EA. Separate neural subsystems within “Wernicke’s area.” Brain 2001; 124: 83-95

Cross References

Agnosia; Agraphia; Alexia; Anomia; Aphasia; Broca’s aphasia; Jargon aphasia; Logorrhea; Paraphasia; Pure word deafness; Schizophasia; Transcortical aphasias

“Wheelchair Sign”

The so-called “wheelchair sign” describes patients with parkinsonism who take to using a wheelchair early in the course of their disease, usually because of falls. Early falls are a feature of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) rather than idiopathic Parkinson’s disease.

Cross References

Parkinsonism; “Rocket sign”

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Wing-Beating Tremor

Wing-Beating Tremor

Wing-beating tremor is absent at rest but develops when the arms are extended, hence a postural tremor. It is said to be typical of Wilson’s disease.

Cross References

Tremor

Winging of the Scapula

Winging of the scapula, or scapula alata, is a failure to hold the medial border of the scapula against the rib cage when pushing forward with the hands. It is most easily observed by asking the patient to push or press against a wall or the examiner’s hand while observing the scapula which lifts away from the posterior chest wall.

Winging of the scapula may be a consequence of weakness of the serratus anterior muscle, usually due to a neuropathy of the long thoracic nerve of Bell, but sometimes as a consequence of brachial plexus injury or cervical root (C7) injury. It may also be of myopathic origin, as in facioscapulohumeral dystrophy.

Weakness of trapezius, particularly the middle trapezius muscle, may also cause winging of the upper part of the scapula, more prominent on abduction of the arm, when the superior angle of the scapula moves farther from the midline. Hence spinal accessory (XI) nerve palsy enters the differential diagnosis.

Witzelsucht

Witzelsucht refers to excessive and inappropriate facetiousness or jocularity, a term coined in the 1890’s for one of the personality changes observed following frontal (especially orbitofrontal) lobe injury. This phenomenon may overlap with those described as moria or emotional lability.

Cross References

Emotionalism, Emotional lability; Frontal lobe syndromes; Moria

Woltman’s Sign

Woltman’s sign denotes slow-relaxing, or “hung-up,” tendon reflexes. These are most commonly seen in the context of untreated hypothyroidism, but have also been recorded in other situations, including treatment with β-blockers, diabetes mellitus, and complete heart block. The phenomenon is sometimes labeled pseudomyotonia because of its superficial resemblance to the slow muscle relaxation of myotonia, but electrophysiological testing does not show myotonic discharges.

Chorea may result in apparently “hung-up” reflexes, perhaps due to a choreiform jerk after muscle relaxation.

The mechanisms underlying Woltman’s sign are uncertain: changes in basal metabolic rate and in muscle fibre types (selective loss of fast twitch fibers) have been suggested.

References

Larner AJ. Normalisation of slow-relaxing tendon reflexes (Woltman’s sign) after cardiac pacing for complete heart block. British Journal of Clinical Practice 1995; 49: 331-332

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Wry Neck

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Cross References

Chorea, Choreo athetusis; Myotonia; Pseudomyotonia

“Wrestler’s Sign”

This name has been given to the excessive effort in irrelevant muscle groups accompanied by prominent verbal grunts in patients with apparent (“functional”) weakness. It may coexist with intermittent voluntary effort, collapsing weakness, co-contraction of agonist and antagonist muscles and inconsistency in clinical examination (e.g., inability to lift leg from couch when recumbent, but able to stand and walk).

Cross References

Collapsing weakness

Wrist Drop

Wrist drop describes a hand hanging in flexion due to weakness of wrist extension. This results from radial nerve palsy, either in the axilla or spiral groove of the humerus (“Saturday night palsy”). Distal lesions affecting branches of the posterior interosseous branch of the radial nerve may produce more circumscribed deformity, such as weak extension of metacarpophalangeal joints (“finger drop,” “thumb drop”).

Writer’s Cramp

Writer’s cramp, or graphospasm, is a focal dystonia of the hand in which dystonic posturing is induced specifically by writing: this is the most common task-specific dystonia. The involuntary movements may eventually make it impossible to write with the dominant hand. Learning to write with the opposite hand may only be a partial solution, since it too may become affected. Muscle fatigue may make writing more legible. Writer’s cramp is much commoner than primary writing tremor as a cause of writing difficulty.

Botulinum toxin injections may be of benefit if relatively few muscles are affected. There may be an associated carpal tunnel syndrome.

References

Sheehy MP, Marsden CD. Writer’s cramp – a focal dystonia. Brain 1982; 105: 461-480

Cross References

Dystonia; Fatigue; Tremor

Wrong-Way Eyes

- see PREVOST’S SIGN

Wry Neck

- see TORTICOLLIS

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Xanthopsia

Xanthopsia is a visual disturbance characterized by excessive perception of yellow colors (literally “yellow vision”). It may be associated with use of various drugs including digoxin (especially if levels are toxic), thiazides (especially chlorothiazide), sulphonamides, and barbiturates. The mechanism is uncertain, but one possibility is that this is a partial form of achromatopsia, affecting one color more than others.

It has been suggested that the artist Vincent van Gogh (1853-1890) may have suffered from xanthopsia as a consequence of digitalis toxicity, accounting for the bright yellows in many of his later canvases.

References

Critchley M. Acquired anomalies of color perception of central origin. Brain 1965; 88: 711-724

Cross References

Achromatopsia

Xerophthalmia, Xerostomia

Xerophthalmia, dryness of the eyes, and xerostomia, dryness of the mouth, due to impaired secretion from the lacrimal glands and the salivary glands respectively, often occur together. This may reflect autonomic dysfunction, as for example in Lambert Eaton myasthenic syndrome, or be due to autoimmune disorders, such as Sjögren’s syndrome.

Cross References

Facilitation; Orthostatic hypotension

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Y

Yawning

Yawning is an arousal reflex thought to be generated in the brainstem reticular formation to counteract brain hypoxia; it may precede vasovagal syncope. Excessive or pathological yawning (chasm) is compulsive, repetitive yawning not triggered by physiological stimuli, such as fatigue or boredom. Known associations of yawning include:

Encephalitis Seizures Multiple sclerosis

Tumors of the 4th ventricle, frontal lobes Electroconvulsive therapy Postthalamotomy

Drugs (valproate, imipramine) Neuroleptic withdrawal

Parkinson’s disease, progressive supranuclear palsy, restless legs syndrome, pseudobulbar palsy of motor neurone disease

Although the mechanisms are uncertain, yawning may represent a disturbance of dopaminergic transmission. Levodopa may help.

References

Leonhardt M, Abele M, Klockgether T, Dichgans J, Weller M. Pathological yawning (chasm) associated with periodic leg movements in sleep: cure by levodopa. Journal of Neurology 1999; 246: 621-622 Williams DR. The yawning reflex: an upper motor neuron sign in amyotrophic lateral sclerosis. Neurology 2000; 55: 1592-1593

Cross References

Parkinsonism; Sighing

Yo-yo-ing

Yo-yo-ing is a form of dyskinesia experienced by patients with idiopathic Parkinson’s disease who have been treated for several years with levodopa preparations, in which there are sudden and unpredictable swings between hypokinesia/akinesia (“off ” state; freezing) and severe hyperkinesia (“on” state), sometimes known as the “on-off phenomenon.” Yo-yo-ing is difficult to treat: approaches include dose fractionation, improved drug absorption, or use of dopaminergic agonists with concurrent reduction in levodopa dosage.

Cross References

Akinesia; Dyskinesia; Hypokinesia

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Zooagnosia

The term zooagnosia has been used to describe a difficulty in recognizing animal faces. This may be observed as a component of prosopagnosia. In one case, this deficit seemed to persist despite improvement in human face recognition, suggesting the possibility of separate systems for animal and human face recognition; however, the evidence is not compelling.

References

Assal G, Favre C, Anderes J. Non recognition of familiar animals by a farmer: zooagnosia or prosopagnosia for animals. Revue Neurologique (Paris) 1984; 140: 580-584

Cross References

Agnosia; Prosopagnosia

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