603 RECOVERY FROM PROLONGED OLIGURIA IN ACUTE GLOMERULONEPHRITIS SIR,-Dr. Persoff (Feb. 13) deserves congratulations One may, on the successful management of his case. however, be forgiven for questioning the diagnosis of acute glomerulonephritis for the following reasons: 1. The early onset of exceptionally severe oliguria (a cupful of urine daily) within 7 days of the beginning of a sore throat. constitutional disturbance, including hiccups and aching muscles. 3. The absence of anasarca and hypertension in the presence of fluid retention severe enough to cause pulmonary oedema. 4. Loin tenderness. 5. A high serum-globulin level. 6. The description and illustration of the renal biopsy appearances with emphasis on interstitial rather than glomerular change. (Glomerulonephritis with prolonged oliguria generally shows more advanced glomerular damage.) 7. The total disappearance of proteinuria by the 55th day of the illness. 2. The
Liverpool Regional Urological Centre, Sefton General Hospital, Liverpool, 15.
H. J. GOLDSMITH.
ABDOMINAL PAIN OF SPINAL ORIGIN
SIR,-In his letter (Feb. 20) Dr. Sjoberg drew attentior
syndrome chondrodynia ". a
which
he
called "
thoracomargina:
Does he include " clicking cartilage " ? This is a conditior which I have seen only in young adults. There is pain anc tenderness over the end of a mobile rib cartilage as Sjôberg describes, though in my experience it has been the 8th or 9th, The pain is actually produced when the tip of the cartilage snaps across the lower border of the cartilage lying immediately superior to it, and with which it would normally articulate or fuse. Local anxsthetics have sometimes helped, but excisior of the distal portion of the offending cartilage has been more effective. This is one of the simple conditions (such as " pulled elbow ") of which I was quite unaware until some years aftei qualification. There must be quite a number of others, which are perhaps better known to manipulators, and to athletes and their trainers, than they are to the recently graduated doctor.
The patient will will but listen. Medical
frequently
tell
us
the
diagnosis if
we
JOHN M. MYNORS.
College, Mosul, Iraq.
SIR,-Mr. Daintree Johnson (Feb. 6) writes that he frequently encounters patients with persistent subcostal pain which defies diagnosis who are commonly referred to surgical clinics for dyspepsia or " ? gallstones ". ;
"
"
He presumes many must be cases of prolapsed dorsal intervertebral disc. Dr. Barbor (Feb. 20) agrees with this point of view, and his treatment is aimed at reducing the protrusion by manipulation or spinal traction. While
agreeing
that these
physical
measures are
often
suc-
cessful, I must disagree with the oversimplification of the underlying pathology and the present fashion of putting all the blame on the unfortunate disc. Although sometimes the result of genuine nuclear prolapse, in my opinion the symptoms are more frequently due to apophyseal, costo-vertebral, or costo-transverse arthritis which gives rise to referred pain. In the thoracic region, as elsewhere, disc degeneration, which is very different from nuclear prolapse, leads to narrowing of the affected disc. This not only causes the facets of the associated posterior joints to override but also the costo-vertebral articulations, the facets on the rib-heads overriding the corresponding facets on the
E. J. CRISP.
London, W.l.
AN UNUSUAL VARIETY OF MUSCULAR DYSTROPHY
severe
None of these points in isolation contradicts the In combination they render it author’s diagnosis. The of leptospiral nephritis or alternatives questionable. allergic interstitial nephritis should be considered.
to
vertebral bodies1 and, in due course, leading to arthritic changes. When this is so, manipulation or traction provides relief, not by reducing a nuclear protrusion but by stretching a sensitive intervertebral, costo-vertebral, or costo-transverse capsular ligament from which the referred pain arises.
SIR,-I must thank Dr. Blyth (Feb. 13) for pointing out the slip in my article concerning her joint Yorkshire survey. Fortunately it does not alter the argument since all the girls in her series fell into the " mild group " who were usually still walking at the age of 11 years. I am not sure whether Dr. Ray (Feb. 13) infers that the cases I described might be " amyotonia congenita ". I gather the term was first used in the articles of Oppenheim 2 and Collier and Wilson,3and I understand that Oppenheim’s cases were non-progressive and that there was no familial incidence. The sisters I have described do not, therefore, conform to this
original description. The section of Ford’s Neurology of Childhood referred to by Dr. Ray mentions changes in the spinal grey matter in associa-
tion with amyotonia congenita. Pathological material was not available to Oppenheim, but the only abnormality found in the central nervous system of the first sister was an unusual hardness of the frontal lobes without microscopic changes. Furthermore, the electromyograms on both children favoured a myopathy rather than a neurogenic atrophy. Ford, however, continues in the same section: " Brandt’s careful study has led to the conclusion that amyotonia congenita is no more than a syndrome. In most instances in which this diagnosis is made we are dealing with Werdnig-Hoffmann’s progressive spinal atrophy... A small percentage of cases are due to myopathy, sometimes the congenital (non-progressive) myopathy of Turner." Thus, in one section the term is given a specific histological pattern and in the next it is said to be no more than a syndrome. Walton 4 equates amyotonia congenita with the syndrome of the floppy child and says 5: " The term ... should be discarded unless it is taken to mean the clinical syndrome of infantile hypotonia without any prognostic implications." Raze 6 makes a plea " to discard the confusing term ... At present it is generally agreed that amyotonia congenita is a symptom complex which is common to some examples of infantile progressive muscular atrophy (Werdnig-Hoffmann), congenital myopathy and infantile polyneuritis ". There seems to be substantial agreement that amyotonia congenita, if the term is to be used at all, should be applied to the symptom-complex of the floppy infant. As such, it is a clinical term and no specific histological pattern can be ascribed to it. If one continues to use the term it will include a variety of pathological entities varying from, perhaps, early dyskinetic cerebral palsy to rod body myopathy, but, like the " nephrotic syndrome " or the " malabsorption syndrome ", it does not infer any one particular diagnostic entity. Oppenheim pointed to the benign prognosis of his group, which may have included examples of what we now call benign congenital hypotonia and early onset non-progressive muscular dystrophy. It is unfortunate that the term has been used outside this context. I would conclude therefore that: 1. The two sisters do not conform to Oppenheim’s original clinical description. 2. The pathological features in the central nervous system which Ford ascribes to amyotonia congenita were not found in the first sister. 1. Crisp, E. J. Disc Lesions and other Intervertebral Derangements; p. 69. Edinburgh, 1960. 2. Oppenheim, H. Mschr. Psychiat. Neurol. 1900, 8, 232. 3. Collier, J., Wilson, S. A. K. Brain, 1908, 31, 1. 4. Walton, J. N. J. Neurol. Psychiat. 1957, 20, 144. 5. Walton, J. N. Lancet, 1956, i, 1023. 6. Rabe, E. F. J. Pediat. 1964, 64, 422.