Neurology Flashcards
Describe the order of the neurological exam?
- Sensorium. 2. Cranial nerves. 3. Gait. 4. Postural reactions. 5. Spinal reflexes.
Why do a neurological examination?
To determine if the nervous system is affected in a disease process, to establish an anatomic diagnosis - forebrain (prosencephalon), pons and medulla, cerebellum, C1-C5 spinal cord, C6-T2 spinal cord, T3-L3 spinal cord, L4-Cd Spinal cord, neuromuscular.
What are the signs of forebrain disease in sensorium?
Check behaviour, mental status. Changes in sensorium may be dullness, lethargy, obtundation, semicoma, stupor, coma, central blindness, abnormal limb placement, circling (often towards the lesion), seizures.
How do you check the cranial nerve reflexes?
Menace - check vision and pupils (may be ANiscoria) Check PLR
Eye position/movement
Nystagmus - named after the direction of the fast phase. fast phase away from lesion. horizontal and rotatory nystagmus - peripheral disease. Vertical nystagmus - central lesion.
Palpebral response
Nasal septal response
Muscles of mastication
Gag reflex.
What may be present in the gait on a neurological exam?
Vestibular/cerebellar/GP ataxia
UMN/LMN paresis;
UMN - delay in the onset of protraction/spasticity
LMN - inability to support weight
Ataxia - general proprioception, vestibular, cerebellar
Which postural reactions should be checked in a neurological exam?
Palpate limbs, paw placement, hopping responses on Pelvic and thoracic limbs and hemiwalking.
Which spinal reflexes should be tested on neurological examination?
Cutaneous trunci reflex, perineal reflex, patellar reflex, withdrawal reflex/nociception.
What are the clinical signs of forebrain Disease?
Abnormal behaviour, head pressing, staring at walls, getting stuck in corners, abnormal mental status, circling in wide circles towards the side of the lesion, continuous pacing, normal gait, Contralateral postural deficits, central blindness (contralateral to the lesion), sensory deficits (contralateral to the lesion), generalised or/and partial seizures, adversive (hemineglect) syndrome, hippus or pupillary athetosis, abnormal temperature regulation, abnormal appetite, abnormal sleep wake cycle, endocrine disturbances - diabetes insipidus, diabetes mellitus, hyperadrenocorticism, acromegaly (excess of growth hormone).
What diagnostic procedures an be done for forebrain disease?
Physical and neurological examination, MDB, EEG, CT scan or MRI, CSF analysis, infectious disease titres on serum/CSF, biopsy.
Describe storage diseases of the forebrain?
Degenerative disorders characterised by the accumulation of different products of cell metabolism within lysosomes. One or more defective enzymes. Accumulation of by products leads to cellular and organ dysfunction. Progressive myoclonic epilepsy (lafora diseasE) in miniature wire haired dachshuds, beagles and basset hounds, fucosidosis - english springer spaniels, ceroid lipofuscinosis - english setters, broder collies, tibetan terriers.
Describe hydrocephalus
Increased CSF volume in dilated ventricular cavities. Compensatory hydrocephalus or Ex vacuo. Non communicating or obstructive hydrocephalus, communicating hydrocephalus - increased production of CSF or decreased CSF reabsorption. Congenital hydrocephalus - chihuahua, Yorkshire terrier, pomeranian, pekingese, english bulldog, pug. Presents - large domed head, lateral or ventrolateral strabismus, persistent sutures and fontanelles, loss of trained habits, seizures, blindness.
Describe the diagnosis and treatment of congenital hydrocephalus?
EEG, brain ultrasound through open fontanelle, skull radiographs, brain ct scan or MRI. Treat with furosemide, corticosteroids, acetazolamide. Or surgically with ventriculoperitoneal shunt.
Which metabolic disorders can cause diseases of the forebrain?
Hypoglycaemia, organ dysfunction - hepatic or uraemic encephalopathy. Endocrine diseases - diabetes mellitus, hypothyroidism, hyperthyroidism. Electrolyte imbalances - hyponatraemia, hypernatraemia, hypophosphtaemia, hypercalcaemia, acidosis or alkalosis.
What is hepatic encephalopathy?
seen with Acquired (acute or chronic liver failure), or congenital portosystemic shunt. Toxic substances from intestinal degradation are not metabolised by the liver or bypass it, reaching the brain. Causes depression, head pressing, tremors, seizures, central blindness and ataxia. Diagnosis is with bile acids test, abdominal ultrasound, abdominal ct scan, positive contrast portopgraphy, brain MRI, Medical treatment: low protein diet, antibiotics and lactulose, surgical ligation.
Describe Neoplastic diseases of the brain seen in dogs
Primary tumours - glioma (astrocytoma and oligdendroglioma), meningioma
Secondary tumours - nasal adenocarcinoma, pituitary macroadenoma, metastasis from mammary prostatic or pulmonary carcinomas or haemangiosarcomas.
Describe neoplastic diseases of the brain seen in the cat
Primary tumours - meningioma
Secondary tumours - metastatic carcinoma, lymphosarcoma, squamous cell carcinoma, nasal adenocarcinoma.
Which infectious organisms cause diseases of the forebrain?
Viruses - Rabies, pseudorabies, CDV, FIP, canine herpes, WNV
Protozoa - toxoplasmosis, neosporosis
Rickettsia - RMSF, Ehrlichia canis
Fungi -Cryptococcis, blastomycosis, histoplasmosis, coccidiomycosis.
Parasites - cuterebra, coenurus, cystercercs, dirofilaria immitis, toxocara canis.
Bacteria - pasteurella spp, s aureus, s. epidermis
Spirochetes - leptosirosis, (Lyme disease).
Protothecosis.
What signs does Canine distemper virus causE?
In young dogs, CNS signs may occur weeks to months after recovery from systemic illness, myoclonus: rhythmical jerking movements of muscle groups.
how does Feline infectious peritonitis affect the brain?
the dry/non effusive/granulomatous form. CSF _ mixed pleocytosis (predominantly neutrophils) PCR on CSF. MRI or CT brain - hydrocephalus, meningitis and choroiditis.
Describe inflammatory diseases of the forebrain?
Meningo encephalitis of unknown origin - necrotizing minigo encephalitis of pug and maltese dogs and Yorkshire terrier encephalitis - fore brain signs.
Granulomatous meningo encephalo-myelitis - caudal fossa (cerebellum + pons/medulla) and forebrain signs.
What substances can cause toxic diseases of the forebrain?
Ethylene glycol toxicity, lead poisoning
Describe vascular diseases of the forebrain?
Diffuse cerebral ischaemia - caused by cardiopulmonary arrest, anaesthetic accident, severe cerebral edema following a toxic or traumatic event.
Focal cerebral iscahemia - i.e thrombus, embolism or thromboembolic diseases caused by cardiac disorders, septic or neoplastic emboli,hypothyroidism inducing atherosclerosis (RARE), migrating parasites.
Diffuse or focal haemorrhages caused by trauma, neoplasia, coagulation disorders e.g rodenticide intoxication, severe hepatopathy, vasculitis, hypertension (secondary to hyperadrenocorticism, renal failure).
Describe the pathophysiology of head trauma
Primary injuries - fractures, blood vessel disruptrion, tearing or crushing of parenchyma. Occur at the time of trauma. non reversible.
Secondary injuries - ischaemia, excitotoxicity, cerebral edema (vasogenic edema, cellular or cytotoxic edema), haemorrhage. hours to days after trauma - coontrollable.
Describe what fills th intracranial space?
80% brain, 10% blood, 10% CSF, encased in bone, intracranial pressure is the pressure exerted by tissues and fluids within the cranial vault. Causes of increased intracranial pressure in head trauma : intracranial haemorrhage, cerebral edema, systemic hypotension, hypoxaemia.
What is cushings reflex?
Increased intracranial pressure > cerebral schaemia> increase in heart rate and systemic extra cranial vasoconstriction > reflex systemic hypertension to increase cerebral perfusion > increased systemic arterial blood pressure stimulates baroreceptor reflex inducing bradycardia.
What are the goals of head trauma management and how is neurologic assessment done?
Maintain ventilation, avoid hypotension, prevent/treat cerebral edema, treat increased ICP. Neurologic assessment - state of consciousness, breathing pattern, size and responsiveness of pupils, Occular position and movements, skeletal motor responses.
What are the different levels of consciousness, breathing patterns and occular positions that may be noted in neurological exam after head trauma?
alert, depressed, demented, stuporous, comatose.
Cheyne-stokes respiration (forebrain)
Central neurogenic hyperventilation (mesencephalon/pons)
Apneustic breathing or cluster breathing (pons/medulla)
Ataxic respiration (respiratory centres in medulla).
Abnormal oculocephalic reflex or physiologic nystagmus, strabismus.
What signs may b e present with brainstem injuries?
Abnormal oculocephalic reflex (physiological nystagmus), bilateral unresponsive miotic pupils, mydriasis or asymmetrical pupils, strabismus and other cranial nerve deficits, abnormalities or changes in respiratory pattern.
What is the difference between decerebrate rigidity and decerebellate rigidity?
Decerebrate - unconsciousness, abnormal pupillary function,, opisthotonus, extension of thoracic and pelvic limbs.
Decerebellate rigidity - alert, normal pupillary function, opisthotonus, extension of thoracic limbs, extension or active flexion of pelvic limbs.
What are the clinical signs of Increased ICP?
Nausea/ovomiting, decreased PLR, decreased level of consciousness, Cushings reflex (hypertension & bradycardia) abnormal respiratory pattern, increased limbs’ extensor tone.
What are epileptic seizures?
abnormal brain function, synchronous activation of many neurons or excessive activation of few neurons, in the cerebral cortex. usually self limiting. Epilepsy is a chronic neurologic condition, wit recurrent epileptic seizures.
What are convulsions?
Have a generalised motor component, excessive, abnormal muscle contractions, usually bilateral.
What is ictus?
A sudden neurologic occurence, such as a stroke or an epileptic seizure
What is the prodromal stage and pre ictal phenomenon?
behavioural changes or autonomic signs that may precede an observable seizure.
What is the post ictal phenomenon?
A transient clinical abnormality of the CNS function that appears or becomes more evident when the clinical signs of the seizure have ended e.g disorientation, ataxia, central blindness behavioural changes.
What are generalized seizures?
Have involvement of both the cerebral hemispheres - tonic clonic seizures, clonic, tonic, atonic or absence seizures.
focal or partial seizures activation of only part of a cerebral hemisphere - simple partial seizures (conscioussness is not impaired), complex partial seizures (with impairment of consciousness.)
What is a cluster of seizures?
> two seizures in a 24 hour period or over 2-3 consecutive days.
What is status epilepticus?
A seizure that shows no clinical signs of arresting after 5-10 minutes of activity or recurrent seizures with no recovery between them.
What is idiopathic epilepsy?
Recurrent seizures, no identifiable cause, genetic/familial predisposition, age dependent.
What is symptomatic epilepsy?
Result of identifiable intracranial or extracranial disease. intracranial causes such as brain tumors, encephalitides, infarcts.
Extracranial diseases such as toxic or metabolic disorders.
What is a seizure?
A seizure is originated by an imbalance of excitatory and inhibitory influences on the cerebral neurons.. When too many cells in the cerebral cortex become too excited a seizure can result. there is a seizure threshold. There is a seizure foci - paraoxysmal depolarisation in a neuron. There is spread of activity to the surrounding neurons. Propagation of seizure activity to cortical areas by axonal conduction. Generalization of seizure activity through diencephalon and corpus callosum.
What signs may be present in a generalised tonic clonic seizure?
Loss of conscioussness, opisthotonus, piloerection, chewing movements, face twitching, midriasis, salivation, apnea, lateral recumbency, urination/defecaetion. tonic phase is stiff legs and clonic phase is paddling legs.
Which dogs are predisposed to idiopathic epilepsy?
Between 105 yerars, regular intervals initially > 4 weeks.Genetic basis of epilepsy in beagles, german shepherd dogs, keeshonds, golden and Labrador retrievers, bernese mountain dogs, tervuren elgian shepherds, viszla, english springer spaniels, border collies, finnish spitz dogs.
What is the DDx for Idiopathic epilepsy?
Syncope (cardiac arrythmias, induced by changes in posture or excercise) sleep disorder (short duration and rapid reovery, occurs only during sleep, attacks can be interupted by awakening), Obsessive compulsive behaviour (prolonged duration of signs, behaviour can be interupted, no impairment of conscioussnes), scotty cramp (breed specific, excercise or stress induced), canine distemper myoclonus (continuous abnormal movements, no impairment of consciousnes), myasthenia gravis (gradual onset and recovery, no loss of conscioussness), vestibular disease (prolonged duration of signs), tremor disorders (prolonged duration of signs, no impairment of consciousness) Narcolepsy/cataplexy (attacks often induced by ecitement, food, play, reversed by external stimulation.
How is IE diagnosed?
Signalment History Physical and neurological examination CBC, biochemical panel, UA Bile acids, lead level, serological studies, thyroid panel, EEG, CSF analysis, CT scan or MRI.
What is the aim in treatment of IE and the expectations?
Reduction in frequency and intensity of seizures
Rarely will become seizure free
owner should keep a seizure log
anti epileptic therapy must have regular administration, do not stop suddenly AE therapy, has side effects, kindling phenomenon
How can epilepsy be treated by vagal nerve stimulation?
A surgically implanted device (neck area) prevents seizures stimulating the left vagal nerve and desychronizing the cortical neurons. Reasonable margin of safetly. well tolerated. reduction in seizure frequently in some dogs.
What medicines should not be used in epileptic animals??
Some drugs such as metoclopramide, penicillin, chloramphenicol, Enrofloxacin and estrogens or testosterone may lower the seizure threshold. Phenothiazines are reported to induce seizures, however acepromazine appears to be safe for use in dogs with epilepsy.
What is the treatment of status epilepticus?
Stop the seizure - use diazepam per rectum to stop a seizure. May repeat 2 more times at 5 minute intervals. Injectable form of diazepam may be more effective than supositories. Alternatives with no IV access, midazolam or dexmedetomidime Im. Place an IV catheter. collect blood for haematology and biochemistry and antiepileptic drug serum level in case the patient is already receiving AED. If diazepam stops the seizure only for a short period of time - use phenobarbitone and repeat 3 more times at 1-6 hour intervals. Levetiracetam also can be used for patients with hepatopathy or PSS. If 3 doses of diazepam are not sufficient to stop the seizure - administer propofol then switch to a CRI of propofol. Monitor cardio respiratory function closely and be ready to intubate if necessary.
What are the requirements for anti epileptic drugs?
Successful control of seizures with anticonvulsant drug reflects a balance between achieving seizure control and minimising side effects.May only be able to increase the seizure interval. BEneficial since seizures can lead to additional seizuring.
Describe the drug requirements for status epilepticus?
Rapid onset of action, available for i/v usage, minimal effects on cardiovascular and respiratory systems. e.g diazepam - a benzodiazepine is the D.O.C. Phenobarbital, propofol.
What are the drug requirement for maintenance therapy?
Long duration of action (once daily treatment), good oral absorption and passage through the BBB, metabolic tolerance limited, minimal sedation, consistent clinical response, absence of major side effects (hepatotoxicity). All available drugs fail to meet these requirements.
What are the mechanisms of action of the anti epileptic drugs?
Enhanced GABA (gamma-aminobutyric acid) synaptic transmission - barbiturates, benzodiazepines, imepitoin.
Potassium bromide - distributes to ECF, crosses neuronal Cl- channels more readily than Cl-. GABA enhances this influx of bromide leading to neuronal hyperpolarization thus bromide stabilises neurone against excitatory input from epileptic foci.
Describe the use of phenobarbital for epilepsy
Frequently used in canine epilepsy - first line and licensed. Can be used in cats and horses also. potentiates synaptic inhibition through the GABA receptor. Oral absorption is slow but good it is usually given orally. injectable form also available for status epilepticus management. 25% is excreted unchanged by the kidneys - it acts as a weak acid therefore alkalinisation of urine enhances excretion. the rest is metabolised by oxidative hydroxylation and then glucuronide onjucation. it is a potent inducer of heptatic microsomal enzymes. Effective in about 60-80% of canine epilepsy.
Describe the use of imepitoin for Epilepsy?
new, licensed as a sole agent for canine epilepsy. it is a partial agonist with low affinity for the BDZ binding site of the GABA receptor. certain advantages since low affinity and efficacy. it is targeted - only binds when GABA is present. Oral bioavailability is decreased a little with food but doesnt matter as long as consistency is important. Hepatic metabolism (oxidation) and inactive metabolites undergo faecal excretion. There is no induction of liver enzymes. It has a half life about 2 hours so steady state is rapidly achieved.
Describe how potassium bromide is used as an anti epileptic drug?
Halide element and causes neuronal hyperpolarization by entering neurons via chloride channels. it is synergistic with phenobarbital (licensed for combo treatment), handled like chloride in the body, excreteed in the kidneys ( no biotransformation) half life in dogs 1 months. Steady state - 3-6 months. dietary chloride will influence half life. High chloride diets increase elimination and derease half life (dry diets e.g hills s/d id h/d). Indications are for with phenobarbital for uncontrolled seizures, dogs with hepatotoxicity, pre existing liver disease, unnaceptable side effects of phenobarbital.
Describe the use of diazepam as an anti epileptic drug?
It is a benzodiazepene which enhances the inhibitory effect of GABA in the brain and spinal cord. It is the drug of choice for the management of status epilepticus in the dog and cat. Can be used for long term seizure management in the cat - given orally 12-24hours. It is rapidly metabolised to a variety of active metabolites such as nordiazepam and oxazepam. Species variation on percentage metabolites but metabolites are active. Quite highly bound to plasma protein. Half life has a species variation - 6X longer in cat than dog. Can be given orally or parenterally. Hepatic necrosis in cats seen as early as 5 ays after treatment initiation. This can be rapidly fatal so very serious. Monitor hepatic parameters.
Describe the potential for toxicity in all anti epileptic drugs?
Side effects include - sedation, polyphagia, polydipsia, polyuria
High long term doses of phenobarbital can lead to hepatotoxicity
Asthma like symptoms have been reported in cats on KBr. Gingival hyperplasia occurs occasionally in cats. Most dogs receiving chronic anticonvulsant therapy will develop abnormalities in serum biochemistry and hepatic function tests.
What should the dosing schedule be for anti epileptic drugs?
Dosage requirements of anti epileptic drug vary between patients and should be determined on an individual basis. Dosage depends on the incidence and severity of seizures. Initial daily dose requirement may have to be increased to maintain blood and brain concentrations as a consequence of metabolic tolerance (liver enzyme induction). Pharmacokinetics data help to establish dialy dosing regimens - good for dog, sparse for cat. For both dog and cat, when complete control of seizures for 6 months, careful stepwise reduction in drug dosage may be attempted.
How can anti epileptic drugs be used in combination therapy?
Select drugs from differing classes eg phenobarbital and potassiu, bromide. approx 30% of dog are refractory to phenobarbital or side effects are unacceptable - sedation, hepatotoxicity. Control is particularly difficult in dogs with cluster fits - there is an apparent high incidence of refractory epilepsy in GSDS. Use 2 drugs in combination if a single agent causes toxicity or has failure to control (e.g seizures once per 2 weeks). Avoid irrational combinations e.g phenobarbital and primidone, phenobarbital and phenytoin (metabolic toelrance).
Describe epilepsy in the cat
Much less common than in the dog, more often reflects structural disease, less pharmacokinetic data and extrapolation is not ideal, metabolic tolerance to phenobarbital does not occur, KBr has been tried, diazepam has been used for maintenance therapy in the cat - longer half life.
What is zonisamide?
A new advance - blocks voltage dependent sodium and potassium channels. it has a half life 15 hours in the dog, In a trial on 13 dogs - it was used as an add on treatment, very epensive, promising results but some suggestion of tolerance.
What are gabapentin and pregabalin?
MOA: analogue of GABA but a2 component of calcium channels. they have a short half life, used as an adjunct. Small trial information improvement suggested. Neuropathic pain role in therapy.
What is the function of the vestibular system?
it is responsible for maintaining balance, regulating the position of the eyes, trunk and limbs in relation to changes in position of the head. Maintaining balance depends on - vestibular receptors, vision, proprioceptive receptors in joints and tendons.
Describe the anatomy of the peripheral vestibular system?
Vestibular receptors in utricle and saccule and semicircular canals. Vestibular nerve is CN VIII.
Describe the anatomy of the central vestibular system
Central vestibular system made up of: vestibular nuclei, caudal cerebellar peduncle, fastigial nucleus of the cerebellum flocculonodular lobe of cerebellum.
What are the clinical signs of vestibular disease?
Head tilt,
Nystagmus: involuntary rhythmic oscillation of the eyes - pendular or jerk n, physiologic nystagmus (oculovestiular response), horizontal, fast phase in the direction of the movement. A pathologic nystagmus can be resting nystagmus or positional nystagmus - horizontal, rotatory, vertical. The fast phase is away from the side of the lesion. Vestibular ataxia - falling, rolling, staggering, tight circles towards the side of the lesion, decreased extensor tone ipsilateral limbs, increased extensor tone in contralateral limbs, vomiting and nausea - acute vestibular disease, projections to the emetic centre within the medullary reticular formation, ventral or ventrolateral strabismus, cranial nerve deficits, horners syndrome, hemiparesis and conscious proprioceptive deficits
How can you differentiate peripheral vs central vestibular disease?
Central vestibular disease - conscious proprioceptive deficits, vertical resting or positional nystagmus, nystagmus changing direction with changes in head position, cranial nerve deficits other than CN VII, cerebellar signs, decreased level of conscioussness, paradoxical vestibular syndrome.
What is paradoxical vestibular syndrome?
Contradictory vestibular signs caused by loss of cerebellar inhibition of the vestibular output.
What are the clinical signs of bilateral vestibular disease?
Absent physiologic and or pathologic nystagmus, absent head tilt, side to side swaying of the head, broad based stance, falling to either side,
What diagnostic procedures can be used for vestibular disease?
Physical, neurological, otoscopic and pharyngeal examination. haematology and biochemistry, skull radiographs, CT scan or MRI, ear cytology, ear culture and sensitivity, myringotomy, CSF analysis, infectious diseases titers on serum and or CSF, biopsy/histopathology,
Describe the anomalous causes of peripheral vestibular disease
Bilateral congenital vestibular disease seen in akitas, beagles.
Congenital peripheral vestibular disease in GSDs, dobermans, english cocker spaniel, siamese cat, burmese cat.
Describe the metabolic causes of peripheral vestibular disease?
Hypothyroidism - associated with various neurological signs from seizures to mega esophagus, ,laryngeal and facial nerve paralysis. Mucinous deposits in and around facial and vestibular nerve may cause compression of the axons as they pass through the internal acoustic meatus of the temporal bone.
What are the neoplastic causes of Peripheral vestibular disease?
Squamous cell carcinoma (cat, ceruminous gland adenoma (dog and adenocarcinoma (cat), papillary adenoma (dog), lymphosarcoma, osteosarcoma, chondrosarcoma, fibrosarcoma.
How may iatrogenic vestibular disease be caused?
Chlorhexidine, aminoglycosides.
Streptomycin and gentamycin > vestibular receptors.
Neomycin, kanamycin and amikacin > auditory receptors.
What are the infectious & inflammatory causes of peripheral vestibular disease?
Infectious: otitis media interna,
inflammatory polyps.
What is idiopathic canine geriatric vestibular disease?
It is acute, idiopathic, peripheral vestibular disease which causes vomiting, nausea and severe vestibular deficits. Spontaneous improvement in 3-2 days. Usually normal in 7-10 days in some cases up to 2-3 weeks and sometimes there is a residual head tilt. recurrence is possible. No treatment.
What are the causes of central vestibular disease?
Denegerative: inherited lysosomal storage diseases
Anomalous - arachnoid cyst, cerebellar cyst, hydrocephalus
Neoplastic - primary: meningioma, choroid plexus tumour, ependymoma, nerve sheath tumour, glioma. Secondary : lymphosarcoma, hemaengiosarcoma, prostatic or mammary carcinoma. nutritional:thiamine deficiency. Iatrogenic: traumatic cisternal spinal tap.
Name the infectious organisms that can cause central vestibular infectious diseases?
Viruses - rabies, pseudorabies, CDV, parvovirus, parainfluenza, herpes. Protozoa - toxoplasmosis, neosporosis
Rickettsia - RMSF, ehrlichia canis
Fungi - cryptococcos, blastomycosis, histoplasmosis, coccidiomycosis, aspergillosis.
Parasites - cuterebra, coenurus, cystercerus, dilofileria immitis, nematodes. Bacteria - pastuerella sp, s aureus, s. epidermis, l monocytogenes. Spirochetes - leptospirosis.
Other - protothecosis.
What is granulomatous meningoencephalomyelitis? (GME)
Sunacute to chronic sterile inflammation, suspected immune mediate ddisorder. Female middle age small breed dogs. Disseminated focal and ocular (optic neuritis) form. Prognosis guarded to poor. Definitive diagnosis: histopathology. Traditional treatment: immunosuppresive doses of corticosteroids. Prologned survival time with other immunosuppresive agents in addition to prednisolone such as cytarabine, cyclosporine, procarbazine.
