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SAMJ F ORUM
Discussion
The diagnosis of lingual abscess in the anterior two-thirds of the tongue is simple in view of the characteristic symptoms and signs.1Our patient’s initial diagnosis was confused, possibly because of his lack of communication and the fact that he was apyrexial. Hereditary angioneurotic oedema, caused by C1 esterase inhibitor protein deficiency, usually presents with a triad of symptoms and signs, namely abdominal pain,
peripheral non-pitting oedema, and laryngeal oedema.2 Lingual abscess is an extremely rare condition.3The tongue is very resistant to infection due to factors such as a thick keratinised epithelial layer, resistance of muscle to infection, cleansing action of saliva, abundant vascularity, paucity of submucosal areolar tissue, and contact exposure of the tongue to bacteria resulting in immunity.4The aetiological factors in the formation of tongue abscesses include dental or foreign body trauma,4acute parenchymous glossitis, infected circumvallate papillae, upper respiratory tract infections,5and carious teeth as present in our patient. The symptoms include severe tongue pain, decreased movement of the tongue (protrusion), hyper-salivation, dysphagia and voice change.1
The most common site is the anterior two-thirds of the tongue.4 Abscesses of the lingual tonsil, extension of infections from the molar teeth,6and intralingual thyroglossal duct cysts need to be borne in mind when an abscess is located within the tongue base.3Pyrexia is not necessarily present7and the WCC and ESR are variable.6,7The organisms responsible are usually
Staphylococcus aureus and Streptococcus haemolyticus.4Both ultrasound3(US) and computed tomography (CT)1have been utilised to aid diagnosis.
As in our patient with tongue abscess and delay in diagnosis, treatment includes incision and drainage, airway monitoring, antimicrobial therapy, and addressing causative factors.
1. Redleaf M. Lingual abscess. Ann Otol Rhinol Laryngol 1994; 103: 986-987.
2. Kerr AG. Scott-Brown's Otolaryngology. 6th ed. Oxford: Butterworth-Heinemann, 1997: 5-6.
3. Ossamer JY, Cherry JR, Dalziel M. Lingual abscess: the value of ultrasound in diagnosis. J Laryngol Otol 1989; 103: 950-951.
4. Agarwal KK, Chhangani DL, Bhattacharyya S. Lingual abscess-aetiopathogenesis. J Laryngol Otol 1966; 80: 1038-1040.
5. Newman RK, Johnson JT. Abscess of the lingual tonsil. Arch Otolaryngol Head Neck Surg 1979;
105:277-278.
6. Sands M, Pepe J, Brown RB. Tongue abscess: case report and review. Clin Infect Dis 1993; 16:
133-135.
7. Jain HK, Bhatia PL. Lingual abscess. J Laryngol Otol 1970; 84: 637-641.
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Arteriovenous malformations (AVMs) of the brain are an important although infrequently diagnosed cause of epilepsy.
They may be associated with epilepsy that is difficult to control medically but that may be amenable to surgical control.
A 43-year-old man presented with a history of sudden onset of a very severe headache, nausea, vomiting and transient photophobia. He was neurologically intact. He reported being epileptic for the past 18 years, suffering attacks of grand mal fits approximately 2 - 3 times every month. The cause of his epilepsy had never been investigated although he had been placed on various anti-epileptic drugs with little success. At presentation he was taking three different anti-convulsant drugs. A computed tomography (CT) scan of the brain
demonstrated a bleed in the left frontal lobe, with areas of serpiginous enhancement on contrast administration (Fig. 1).
Digital subtraction angiography revealed the presence of an AVM, supplied by feeders from the left anterior and middle cerebral arteries, and draining into the superior sagittal sinus (Figs 2 and 3). EEG examination did not reveal any other epileptogenic focus in the brain. The lesion was completely resected at craniotomy and the associated blood clot was drained. Following surgery, there was a dramatic improvement in the frequency of the seizures. Apart from one grand mal fit shortly after the operation, he has remained free of fits over a period of several months’ follow-up and has been weaned down to single-drug treatment.
Discussion
Epilepsy in Africa is a common neurological problem although the incidence and prevalence are not accurately known.
Superstition and misconceptions about the disease are rife and often hinder affected individuals from seeking medical attention.
C
LINICALI
MAGESArteriovenous malformations of the brain — curable epilepsy
John R Ouma
The author is a senior specialist neurosurgeon a Johannesburg General Hospital and the University of the Witwatersrand. He holds an MMed in neurosurgery and is a Fellow of the College of Neurosurgeons of South Africa. Although engaged in all areas of neurosurgical practice, he is especially interested in the neurovascular, neuro-oncology and spine fields.
SAMJ F ORUM
The many causes of non-idiopathic epilepsy include congenital infections, perinatal complications including birth trauma and asphyxia, and later in life, trauma with head injury.
Infections such as neurocysticercosis and tuberculosis are important causes, as is HIV, both primarily and as a result of
opportunistic infections and neoplasms. Primary and secondary brain tumours, and neurovascular conditions such as aneurysms and AVMs, are also causes of this condition.
AVMs of the brain are congenital lesions formed by disordered arteries and veins. The clinical presentation of symptomatic AVMs is varied. The commonest presentation is haemorrhage, occurring in about half the patients, while about 30% present with epilepsy.1 A study involving 280 cases of cerebral AVMs2showed that patients with small (< 3 cm) lesions are more likely to present with haemorrhage, while those with larger ones frequently present with epilepsy. Other modes of presentation include progressive neurological deficits arising as a result of pressure exerted by the lesion on neigh- bouring parts of the brain and blood being shunted away from these areas. The natural history of this condition has been described in a comprehensive study.3 The authors reported a major re-bleeding rate of 4.0% per year, and a mortality rate of 1.0% per year. The combined rate of major morbidity and mortality was 2.7% per year. The proposed mechanisms of epilepsy in AVMs include focal cerebral ischaemia due to arteriovenous shunting, gliosis of the surrounding brain and a secondary epileptogenesis in the temporal lobe.4Spontaneously thrombosed AVMs in patients with no previous history of haemorrhage have been associated with intractable seizure disorders.5
Reports of the control of epilepsy following AVM surgery have been encouraging. In a large series283% of those patients with pre-operative epilepsy were seizure free and of those still experiencing seizures, the majority reported significant improvement following surgery. Of those who did not have pre-operative epilepsy, 6% went on to develop it. The mean duration of follow-up in this study was 7.5 years. Excellent results have been reported in other studies,3, 6, 7but a sobering report8suggests that by 20 years after surgery, there is a 57%
risk of epilepsy in patients who had no seizures before.
Surgery generally offers good prospects for the management of epilepsy in patients with AVMs of the brain. It is also favoured because of the cumulative risk of major morbidity and mortality from haemorrhage of these lesions, especially in younger patients.
1. Itoyama Y, Uemura S, Ushio Y, et al. Natural course of unoperated intracranial arteriovenous malformations: study of 50 cases. J Neurosurg 1989; 71: 805-809.
2. Piepgras DG, Sundt TM jun., Ragoowansi AT, Stevens L. Seizure outcome in patients with surgically treated cerebral arteriovenous malformations. J Neurosurg 1993; 78: 5-11.
3. Ondra SL, Troupp H, George ED, Schwab K. The natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. J Neurosurg 1990;
73:387-391.
4. Yeh HS, Kashiwagi S, Tew JM jun., Berger TS. Surgical management of epilepsy associated with cerebral arteriovenous malformations. J Neurosurg 1990; 72: 216-223.
5. Wharen RE jun,, Scheithauer BW, Laws ER jun. Thrombosed arteriovenous malformations of the brain. An important entity in the differential diagnosis of intractable focal seizure disorders. J Neurosurg 1982; 57: 520-526.
6. Yeh HS, Tew JM jun., Gartner M. Seizure control after surgery on cerebral arteriovenous malformations. J Neurosurg 1993; 78 : 12-18.
7. Heros RC, Korosue K, Diebold PM. Surgical excision of cerebral arteriovenous malformations:
Late results. Neurosurgery 1990; 26: 570-578.
8. Crawford PM, West CR, Shaw MDM, Chadwick DE. Cerebral arteriovenous malformations and epilepsy: Factors in the development of epilepsy. Epilepsia 1986; 27: 270-275.
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May 2004, Vol. 94, No. 5 SAMJ
Fig. 1. Non-contrast CT scan showing an acute intracerebral bleed in the left frontal lobe.
Fig. 2. Angiogram of the left internal carotid artery (arterial phase) showing the left frontal arteriovenous malformation being fed by branches of the anterior and middle cerebral arteries.
Fig. 3. Venous phase of the angiogram shown in Fig. 2, showing drainage of the arteriovenous malformation into the superior sagittal sinus.
