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LIKE PTH
722
passive alternate supination and pronation of the forearm. Minor degrees of spasticity reveal themselves as increased resistance to supination, often associated with a brief "catch". The related pronator sign is equally helpful; the arms are held out horizontally, palms upward. Even mild forearm hypertonia causes the limb to pronate gradually. There is often slight elbow flexion but the limb does not necessarily drift downwards. Weakness is not an early pyramidal feature; slowness of rapid finger movement usually precedes demonstrable weakness of interossei and finger extensors. Carefully obtained tendon reflexes are fundamental; slight asymmetry alone may give a clue, perhaps reinforced by an extensor plantar response on that side. Suspicions of arm reflex asymmetry may be verified by the presence of abnormal hand reflexes—eg, Hoffmann’s sign, in which the thumb flexes in response to an upward snapping movement of the middle finger nail. Having carried out all these manoeuvres, there must be few pyramidal lesions that escape notice. Understandably, any claim for the existence of a new physical sign in the hand is likely to be met with amused scepticism. Nonetheless, "myelopathy hand" has now been described by Ono and colleagues.1 It has two components: (a) the finger escape sign-a patient is asked to hold up the arms, palms face downwards, whereupon the little finger on the affected side passively abducts and cannot be maintained in adduction for more
than 30
s.
At
a more
advanced stage the ulnar three
fingers abduct and full extension at the interphalangeal joints of the ulnar fingers is lost. (b) Inability to grip and release rapidly with the arms extended and pronated. A normal person can grip and release at least twenty times in 10 s. In patients with myelopathy the movement slows down, finger extension is incomplete, and wrist extension is exaggerated. Ono et al believe that failure of synergy between wrist and fingers explains their findings. In their series of 127 patients with assorted cervical problems (spondylosis, tumour, disc protrusion), myelopathy hand was observed in over 90%. 4 patients with cervical cord tumour displayed the signs but none of those with cervical radiculopathy unless muscle weakness was present. In the radiculopathy cases the grip-release test was always normal. If simple cervical radiculopathy progressed to "significant" cord compression the signs of myelopathy hand appeared. Patients with myelopathy hand displayed abnormal hand reflexes (Hoffmann’s and Wartenberg’s signs) and pyramidal signs in lower limbs and had lesions characteristically at C5/6 or above. Ono and co-workers concluded that their sign was especially valuable in early detection of pyramidal tract damage, especially in craniocervical disorders, in which conventional signs may be scanty. None of this story is entirely new. Passive abduction of the little finger has been noted in hemiplegia and termed the digiti quinti signand even earlier Soques3 observed abduction of all fingers on the side of hemiparesis. According to Alter,2the fifth finger tends to abduct in hemiparesis because of "the more tenuous voluntary control of this finger at levels of highest integration". Cortical
1. Ono
K, Ebara S, Fuji T, et al. Myelopathy hand. J Bone Joint Surg 1987; 69-B: 215-29. 2. Alter M, The digiti quinti sign of mild hemiparesis. Neurology (Minneap) 1973; 23: 503-05. 3. Soques MA, Sur le "Phenomene des Interosseux" de la main ou "Phenomene des doigts" dans l’hemiplegie organique. Bull Mem Soc Med Hop Paris 1907; June 28th.
of the little finger is considerably less than that of the thumb and index finger, so it is more vulnerable to disease processes. He makes the interesting point that during the first year of life, when corticospinal myelination is unfinished, fifth finger abduction is defective but by the age of 2, when myelination is complete, the finger adducts normally. Some of these findings will puzzle neurologists, who typically screen the pyramidal system by testing simultaneous abduction of index and little finger. Is finger abduction paresis a later phenomenon once adductor paresis is already established? Weakness of little finger abduction is common in ulnar nerve lesions, but this diagnosis should not cause any confusion: flexion at the metacarpophalangeal joint is not possible in ulnar palsy and the pattern of sensory loss in all but the pure motor, deep branch lesion, is characteristic. Slowness of rapid movement is a well-recognised pyramidal sign, but Ono et al attempt to quantify it with the grip-release test. They do not discuss its specificity-ie, whether similar signs appear with brainstem, capsular, or cortical lesions of pyramidal tracts. It is also possible that passive finger abduction would appear in cerebellar disease, but in the latter case the finger would extend at the metacarpophalangeal joint rather than flex as in pyramidal disorders. They do not quantify the frequency of falsepositive tests in a normal population. Despite some lingering doubts about specificity, the hallmarks of myelopathy hand are easy to elicit and appear in early stages of corticospinal dysfunction-but is another sign really needed?
representation
LIKE PTH HYPERCALCAEMIA is a common complication of malignant disease, even when there are no bony metastases. The resulting syndrome-humoral hypercalcaemia of malignancy (HHM)--is probably best known in association with squamous cell carcinoma of the lung. HHM resembles primary hyperparathyroidism in that there is greatly enhanced bone resorption, usually accompanied by reduced renal phosphate threshold and increased renal tubular calcium reabsorption. However, the tumour product is distinct from parathyroid hormone (PTH) since PTH assays seldom detect raised levels in patients with HHM, moreover, PTH messenger RNA is not found in the tumours. Suva and colleagues, studying a human lung cancer cell-line, have now isolated a protein from the culture medium and have cloned and expressed the complementary DNA. The cDNA clones encode a protein of 141 aminoacids with partial sequence homology with PTH, mainly in the first twenty residues. These features of the molecule not only explain why most PTH assays have not detected raised levels but also why a few antisera detect some "PTH immunoreactivity". Suva et al suggest that duplication of a common ancestor of the PTH gene might explain the origins of the protein. This new hormone has also been detected in cultured human keratinocytes, indicating that it may play a role in normal as well as abnormal calcium metabolism. 1. Suva
LJ, Winslow GA, Wettenhall REH, et al. A parathyroid hormone-related protein implicated in malignant hypercalcemia: cloning and expression. Science 1987, 237: 893-96.
passive alternate supination and pronation of the forearm. Minor degrees of spasticity reveal themselves as increased resistance to supination, often associated with a brief "catch". The related pronator sign is equally helpful; the arms are held out horizontally, palms upward. Even mild forearm hypertonia causes the limb to pronate gradually. There is often slight elbow flexion but the limb does not necessarily drift downwards. Weakness is not an early pyramidal feature; slowness of rapid finger movement usually precedes demonstrable weakness of interossei and finger extensors. Carefully obtained tendon reflexes are fundamental; slight asymmetry alone may give a clue, perhaps reinforced by an extensor plantar response on that side. Suspicions of arm reflex asymmetry may be verified by the presence of abnormal hand reflexes—eg, Hoffmann’s sign, in which the thumb flexes in response to an upward snapping movement of the middle finger nail. Having carried out all these manoeuvres, there must be few pyramidal lesions that escape notice. Understandably, any claim for the existence of a new physical sign in the hand is likely to be met with amused scepticism. Nonetheless, "myelopathy hand" has now been described by Ono and colleagues.1 It has two components: (a) the finger escape sign-a patient is asked to hold up the arms, palms face downwards, whereupon the little finger on the affected side passively abducts and cannot be maintained in adduction for more
than 30
s.
At
a more
advanced stage the ulnar three
fingers abduct and full extension at the interphalangeal joints of the ulnar fingers is lost. (b) Inability to grip and release rapidly with the arms extended and pronated. A normal person can grip and release at least twenty times in 10 s. In patients with myelopathy the movement slows down, finger extension is incomplete, and wrist extension is exaggerated. Ono et al believe that failure of synergy between wrist and fingers explains their findings. In their series of 127 patients with assorted cervical problems (spondylosis, tumour, disc protrusion), myelopathy hand was observed in over 90%. 4 patients with cervical cord tumour displayed the signs but none of those with cervical radiculopathy unless muscle weakness was present. In the radiculopathy cases the grip-release test was always normal. If simple cervical radiculopathy progressed to "significant" cord compression the signs of myelopathy hand appeared. Patients with myelopathy hand displayed abnormal hand reflexes (Hoffmann’s and Wartenberg’s signs) and pyramidal signs in lower limbs and had lesions characteristically at C5/6 or above. Ono and co-workers concluded that their sign was especially valuable in early detection of pyramidal tract damage, especially in craniocervical disorders, in which conventional signs may be scanty. None of this story is entirely new. Passive abduction of the little finger has been noted in hemiplegia and termed the digiti quinti signand even earlier Soques3 observed abduction of all fingers on the side of hemiparesis. According to Alter,2the fifth finger tends to abduct in hemiparesis because of "the more tenuous voluntary control of this finger at levels of highest integration". Cortical
1. Ono
K, Ebara S, Fuji T, et al. Myelopathy hand. J Bone Joint Surg 1987; 69-B: 215-29. 2. Alter M, The digiti quinti sign of mild hemiparesis. Neurology (Minneap) 1973; 23: 503-05. 3. Soques MA, Sur le "Phenomene des Interosseux" de la main ou "Phenomene des doigts" dans l’hemiplegie organique. Bull Mem Soc Med Hop Paris 1907; June 28th.
of the little finger is considerably less than that of the thumb and index finger, so it is more vulnerable to disease processes. He makes the interesting point that during the first year of life, when corticospinal myelination is unfinished, fifth finger abduction is defective but by the age of 2, when myelination is complete, the finger adducts normally. Some of these findings will puzzle neurologists, who typically screen the pyramidal system by testing simultaneous abduction of index and little finger. Is finger abduction paresis a later phenomenon once adductor paresis is already established? Weakness of little finger abduction is common in ulnar nerve lesions, but this diagnosis should not cause any confusion: flexion at the metacarpophalangeal joint is not possible in ulnar palsy and the pattern of sensory loss in all but the pure motor, deep branch lesion, is characteristic. Slowness of rapid movement is a well-recognised pyramidal sign, but Ono et al attempt to quantify it with the grip-release test. They do not discuss its specificity-ie, whether similar signs appear with brainstem, capsular, or cortical lesions of pyramidal tracts. It is also possible that passive finger abduction would appear in cerebellar disease, but in the latter case the finger would extend at the metacarpophalangeal joint rather than flex as in pyramidal disorders. They do not quantify the frequency of falsepositive tests in a normal population. Despite some lingering doubts about specificity, the hallmarks of myelopathy hand are easy to elicit and appear in early stages of corticospinal dysfunction-but is another sign really needed?
representation
LIKE PTH HYPERCALCAEMIA is a common complication of malignant disease, even when there are no bony metastases. The resulting syndrome-humoral hypercalcaemia of malignancy (HHM)--is probably best known in association with squamous cell carcinoma of the lung. HHM resembles primary hyperparathyroidism in that there is greatly enhanced bone resorption, usually accompanied by reduced renal phosphate threshold and increased renal tubular calcium reabsorption. However, the tumour product is distinct from parathyroid hormone (PTH) since PTH assays seldom detect raised levels in patients with HHM, moreover, PTH messenger RNA is not found in the tumours. Suva and colleagues, studying a human lung cancer cell-line, have now isolated a protein from the culture medium and have cloned and expressed the complementary DNA. The cDNA clones encode a protein of 141 aminoacids with partial sequence homology with PTH, mainly in the first twenty residues. These features of the molecule not only explain why most PTH assays have not detected raised levels but also why a few antisera detect some "PTH immunoreactivity". Suva et al suggest that duplication of a common ancestor of the PTH gene might explain the origins of the protein. This new hormone has also been detected in cultured human keratinocytes, indicating that it may play a role in normal as well as abnormal calcium metabolism. 1. Suva
LJ, Winslow GA, Wettenhall REH, et al. A parathyroid hormone-related protein implicated in malignant hypercalcemia: cloning and expression. Science 1987, 237: 893-96.