localized to the caudal colliculi (a, b) and vestibular nuclei (c, d). The paramedian T2-weighted image (e) shows hyperintensity of the caudal colliculi and brainstem nuclei located ventrally to the fourth ventricle.
Fig. 4.5. Transverse T2-weighted MR image of the brain of a domestic short hair cat with thiamine (vitamin B1) deficiency. Note the bilaterally symmetrical hyperintensities localized to the lateral geniculate nuclei. See plate 2 for the histology showing focal haemorrhagic necrotic lesions localized to the lateral geniculate nuclei.
Clinical presentation
Clinical signs include anorexia, vomiting, abnormal mentation, seizures, dilated and unresponsive pupils, absent menace response bilaterally, opisthotonos with increased extensor tone of all four limbs, ataxia, tetraparesis, postural reaction deficits and vestibular dys-function (Garosi et al., 2003; Penderis et al., 2007; Palus et al., 2010). In addition, cervical ventroflexion and hyperesthesia to stimuli have been reported in thiamine-deficient cats. Seizures can progress to coma and death if the thiamine deficiency is not treated.
Diagnosis
A presumptive diagnosis of thiamine (vitamin B1) deficiency is based on dietary history, clinical and MRI findings and response to therapy. MRI findings include bilaterally symmetrical hyperintensity on T2-weighted and FLAIR images localized to the red nuclei, caudal colliculi, vestibular nuclei and cerebellar nodulus in dogs (Figs 4.4a–e) (Garosi, 2003) and to the lateral geniculate nuclei, caudal colliculi, periaqueductal grey matter, medial vestibular nuclei, cerebellar nodulus and facial nuclei in cats (Fig. 4.5; plate 2) (Penderis et al., 2007; Palus et al., 2010). These MRI changes have been reported to resolve following thiamine supplementation (Garosi et al., 2003; Palus et al., 2010). Bilaterally symmetrical hyperintense lesions on T2-weighted and FLAIR images have been reported to affect also the cerebral cortex (parietal, occipital, hippocampal lobe) in cats with thiamine deficiency (Marks et al., 2011). Diagnosis can be confirmed by determining whole blood thiamine concentration by high-performance liquid chromatography. This test is now commercially available in many countries and has replaced the erythrocyte transketolase activity assay because of its superior sensitivity and specificity for thiamine status (Marks et al., 2011). Diet samples can also be submitted for thiamine analysis. Pathologic changes include bilaterally symmetrical spongiosis, necrosis and haemorrhage of upper brainstem nuclei including caudal colliculus, lateral geniculate (Plate 2), medial vestibular and oculomotor nuclei.
Management
Treatment should be instituted immediately for any animal suspected of having thiamine deficiency. Thiamine should be administered at 50–100 mg per dog and 25–50 mg per cat IM, SC or PO every 12–24 h until a response is obtained or another diagnosis is established. Emergency management of seizures can be performed as described in Chapter 24. The underlying cause of thiamine deficiency should be identified and managed. The majority of affected dogs and cats respond rapidly to thiamine supplementation and diet change.
Exogenous Toxic Disorders Causing Seizures
Overview
Numerous exogenous toxins can induce seizures (see Box 3.1, Chapter 3) through different mechanisms including increased excitation, decreased inhibition, and interference with energy metabolism (O’Brien, 1998). Toxins may affect the nervous system directly or indirectly, by affecting other organs whose dysfunction secondarily affects the brain (e.g. HE due to toxin-induced hepatic failure, xylitol-induced hypoglycaemia). This chapter focuses predominantly on toxins with direct effect on the nervous system.
Clinical presentation
The suspicion of toxin exposure is often based on the history and the onset of acute neurological signs (including excitation and hyperactivity or obtundation, stupor, coma, muscle tremors and fasciculations, seizures and ataxia) often associated with vomiting, diarrhoea, salivation, bronchoconstriction, bradycardia or tachycardia and hyperthermia. The source of intoxication is not always obvious to the pet owner, and therefore veterinarians should be proactive in asking questions and mentioning possible sources of intoxication any time the clinical presentation raises the suspicion of toxin exposure. Seizure can occur in clusters or as status epilepticus (e.g. organophosphates, strychnine, mycotoxins) or less commonly may be isolated and recurrent (e.g. lead) (O’Brien, 1998).
Diagnosis
The presumptive diagnosis is often based on the history of toxin ingestion and clinical signs. Definitive diagnosis is made by identification of the toxin in feed or suspect bait material, gastric content from vomitus or lavage fluids, water, blood or urine (for urinary excreted toxins).
Management
Emergency treatment of neurotoxicity involves multiple simultaneous steps, including:
• Systemic stabilization (airway patency, ventilation, oxygenation, normalization of blood pressure, correction of any fluid, electrolyte or acid-base imbalances, management of cardiac arrhythmias);
• Seizure control (see Table 4.1 and Chapters 12 and 24);
• Excessive skeletal muscle tremor control (Table 4.1);
• Decontamination and prevention of further absorption of toxin (Table 4.1);
• Control of body temperature: convective whole body cooling (e.g. wetting the fur, placing a fan near the animal) in hyper-Thermic (≥40°C, 104°F) animals, or gradual warming in hypothermic animals. Body temperature should be closely monitored to avoid inducing hypo- or hyperthermia;
• Administration of an antidote when available;
• Nursing care.
Decontamination
The methods of decontamination and prevention of further toxin absorption depend on the route of entry of the toxin and its metabolic profile.
Cutaneous absorbed toxins
Bathing is the standard method of decontamination for cutaneous exposure to most toxic substances (Rosendale, 2002). The patient should be
