trum of PCP more frequently unmasked with the use of
inhaled pentamidine.
J.W. QUlN,
Registrar,
K. W. BAUMGART,
Registrar,
and

R. J. GARSIA,
Staff Specialist,
Department of Clinical Immunology,
Royal Prince Alfred Hospital,
Camperdown, NSW.

Necrobacillosis

References
1. Fallat R, Lowery S, Fiegal DW, Montgomery AB, Berge J.
Changing patterns of Pneumocystis carinii pneumonia (PCP) on
pentamidine aerosol prophylaxis. In: IVth International Conference on AIDS, Stoekholm. Rook 1, 1988, 7167.
2. Bradburne RM, Bettensohn DB, Opal SM, McCool FD. Relapse
of Pneumocystis can’nii pneumonia in the upper lobes during
aerosol pentamidine prophylaxis. Thorax 1989; 44: 591-3.
3. Abd AG, Nierman DM, Ilowite JS, Pierson RN, Loomis Bell
AL. Bilateral upper lobe Pneumocystis carinii pneumonia in a
patient receiving inhaled pentamidine prophylaxis. Chest 1988:
94; 329-31.

- primary anaerobic septicaemia

We read with interest the report by Golledge et al.’ in
which the clinical features in four patients with Lemierre’s
syndrome are described. Many systems may be involved, as
the authors observe, including the central nervous system.
Wardle et al.’ reported a previously healthy 22-year-old man
who developed frank meningitis with multiple cranial nerve
involvement as part of this syndrome. Scanty Gram-negative
bacilli were seen in the cerebrospinal fluid and anaerobic
culture of the latter and blood yielded a pure growth of
Fusobacterium necrophorum. T h e patient was successfully
treated with penicillin and metronidazole.

P.HUDGSON,
Consultant and Senior Lecturcr in Neurology,
Department of‘ Neurology,
Newcastle General Hospital,
and

H.R. INGHAM,
Consultant Microbiologist, Department of Microbiology,
Newcastle General Hospital, Newcastle upon Tyne, England.

References
1. Golledge GL, Weeramanthri T, Beaman MH, Riley T V .
Necrobacillosis - primary anaerobic septicaemia due to Fusobucterium necrophorum. Aust N Z J Med 1990; 20: 702.
2. Wardle JK, Connolley MJ, Ingham HR, Hudgson P, Snow MH.
Necrobacillosis. (Letter). Br Med J 1984: 288; 1916.

Post-hemiplegic dystonia following right anterior
cerebral artery infarction
The term ‘dystonia’ refers to abnormal fluctuations in
muscle tone produced by abnormal patterns of muscle
co:itraction and includes phasic movements of various
types such as tremors and dystonic spasms. Such abnormalities may be seen in a variety of neurological diseases
and dystonia following hemiplegia is well recognised.’-’
The anatomical basis of dystonia is not known, but radiographic data suggest the basal ganglia and in particular the
putamen as the
A 70-year-old dextral female with difficulty in walking was
seen five months following a stroke. A CT Scan done in India
showed a frontal lobe infarction in the anterior cerebral artery
territory on the right side as indicated in Figure 1 (a-d). Relevant findings on neurological examination revealed minimal
weakness (MRC 4-515) in the arm and 4/5 in the leg and
IXTTERS

hyperreflexia. There was no ankle clonus. There were no
callosal signs. She had intermittent flexion ofher toes curling
u p under the sole which was made worse on standing. T h e
foot remained extended at the ankle on standing and any
attempt to bring the heel down forcefully provoked spasms
of the calf muscles with inversion of the ankle. There was
slow but steady improvement with physiotherapy over a
period of five months.
Dystonia usually appears with improvement of the
hemiplegia, the delay being attributed to an aberrant central
nervous system sprouting consequent to a non-progressive
cerebral insult.’ There is evidence that cortical motor areas
are connected by somatotopically organised pathways to the
putamen which through hrther connections to the thalamus

Aust NZ J Med 1991; 2 1

38 1

Figure I (a)-(d): The CT brain scan shows an anterior cerebral artery infarction involving the right SMA.

sends input back to the premotor area supplementary motor
area and motor cortex. Disruption of the thalamic output
to the frontal cortex may produce dystonia resulting from
the release of premotor control activity from thalamic
control.’ It has also been postulated that dystonia could result
from disconnection of the pathways between the putamen
and thalamus with relative preservation of the corticospinal
pathways.’ Attention is drawn to the role of the supplementary motor area (SMA) in high level motor organisation. The

382

SMA projection to the basal ganglia straddles some of the
loops’ and the output of the basal ganglia via the thalamus
is directed mainly to the SMA.6 It is possible therefore that
dystonia could be induced by lesions occurring anywhere
along the cortico (premotor, SMA, motor)-striato-thalamocortical loop. Our patient shows evidence of damage to the
right SMA sparing the thalamus and caudate-putamen
suggesting that dystonia can result from SMA lesions also.
She had focal dystonia involving the foot and it is not clear

Aust NZ J Med 1991; 21

LETTERS

whether or not the SMA has somatotopic organisation as does
the primary motor c o r t e ~ . ~
N. NAGARATNAM,
Staff Geriatrician, Blacktown Hospital and
Visiting Geriatrician, Westmead Hospital, NSW.

References
1. Marsden CD, Obeso JA, Zarrang JJ, Lang AE. The anatomical
basis of symptomatic dystonia. Brain 1985; 108: 463-83.
2. Burke RE, Fahn S, Gold AP. Delayed onset dystonia in patients
with static encephalopathy. J Neural Neurosurg Psych 1980;
73:789-91.
3. Grimes JD, Hassan MN, Quarrington AM, DAlton J. Delayed-

LETTERS

onset post-hemiplegic dystonia: demonstration of basal ganglia
pathology. Neurology 1982; 32: 1033-5.
4. Koller WC. Letter to editor. Neurology 1985, 35: 615.
5. Weisendanger M, Hummelstein H, Bianchett M cf uf. Input and
output organisation of the supplementary motor area. Motor areas
of the cerebral cortex. Ciba Foundation Symposium, Chichester:
Wiley, 1987.
6. Schell GR, Shrick PL. The origin ofthalamic inputs to the arcuate
premotor and supplementary motor area. J Neurosci 1984; 4:
539-60.
7. Mitz AR, Wise SP. The somatotopic organisation of the
supplementary motor area: intra cortical microstimulation
mapping. J Neurosci 1987; 1010-21.

Aust NZ J Med 1991; 21

383