Editor-In-Chief: C. Michael Gibson, M.S., M.D. 
A febrile seizure, also known as a fever fit or febrile convulsion is a generalized convulsion caused by elevated body temperature. They most commonly occur in children below the age of three and should not be diagnosed in children under the age of 6 months or over the age of 6 years. In many cases, the first sign of fever is the onset of the seizure. It has been theorized that the seizure is triggered by the rapidity of the rise in temperature, rather than the actual temperature reached.
- Seizure less than 15 minutes
- Does not reoccur in same febrile illness
- Focal features
- Prolonged past 15 minutes
- Reoccurs with 24 hours
Febrile seizures represent the meeting point between a low seizure threshold (genetically and age determined) - some children have a greater tendency to have a seizure under certain circumstances - and a trigger: fever. The genetic causes of febrile seizures are still being researched. Some mutations that cause a neuronal hyperexcitability and could be responsible for febrile seizures have already been discovered.
The diagnosis is one that must be arrived at by eliminating more serious causes of seizure: in particular, meningitis and encephalitis must be ruled out. Therefore a doctor's opinion should be sought and in many cases the child would be admitted to hospital overnight for observation and/or tests. As a general rule, if the child returns to a normal state of health soon after the seizure, a nervous system infection is unlikely. Even in cases where the diagnosis is febrile seizure, doctors will try to identify and treat the source of fever. In particular, it is useful to distinguish the event as a simple febrile seizure - in which the seizure lasts less than 15 minutes, does not recur in the next 24 hours, and involves the entire body (classically a generalized tonic-clonic seizure). The complex febrile seizure is characterized by long duration, recurrence, or focus on only part of the body. The simple seizure represents the majority of cases and is considered to be less of a cause for concern than the complex. It is reassuring if the cause of seizure can indeed be determined to have been fever, as simple febrile seizures generally do not cause permanent brain injury; do not tend to recur frequently, as children tend to 'out-grow' them; and do not make the development of adult epilepsy significantly more likely (less than 3-5% which is similar to that of the general public).
Children with febrile convulsions who are destined to suffer from afebrile epileptic attacks in the future will usually exhibit the following:
- A family history of afebrile convulsions in first degree relatives (a parent or sibling)
- A pre-convulsion history of abnormal neurological signs or developmental delay
- A febrile convulsion lasting longer than 15 minutes
- A febrile convulsion with strong indications of focal features before, during or afterward
Early use of antipyretics for fever seems useful and effective. Applying cold (tepid sponging) is no longer recommended, as it does not appear to offer any advantage over antipyretic medications. The commonly given advice to give anti-pyretic drugs to reduce fever in the hope of reducing the risk of febrile convulsion following childhood immunization lacks good evidence of effectiveness.
For children who present with a prolonged seizure, rectal diazepam may be used at home in the event of another prolonged (e.g. more than 5 minutes) seizure is an option. Some children have frequent episodes, and although it is tempting to prescribe anti-epileptic medication to prevent stress and inconvenience, it is hard to justify the risk:benefit ratio.
Following a first febrile convulsion, 2-4% of children will have an unprovoked (i.e. afebrile) seizure - this is 4 x the risk in general population). Most of these children will subsequently develop epilepsy. Other risk factors for developing epilepsy:
- Family history of epilepsy
- Complex features
- Presence of early onset neuro-developmental abnormalities
Genetic basis but multiple chromosomes, so complex and not strictly autosomal dominant. Current opinion supports an association between prolonged febrile convulsion and lesions in the temporal lobe (especially hippocampal sclerosis; in the past it was thought febrile convulsions might predispose to temporal lobe epilepsy, but the brain lesions probably pre-exists and increases the likelihood of febrile convulsion.
Prognosis is generally good. One third of children presenting with a febrile convulsion will have another one (recurrence); age would appear to be the single, strongest, and most consistent risk factor: the younger you are when you have your first, the more likely you are to have another before you grow out of it! Most recurrences will occur during the first year after the initial episode and over 90% recur within two years. Other risks - family history of febrile seizures (but not epilepsy) in a first degree relative, children whose initial seizure occurred with a relatively low fever, multiple initial seizures occurring during the same febrile episode. Surprisingly, status epilepticus in an otherwise normal child does not appear to significantly increase the risk for further febrile seizures or the development of epilepsy.
|Diseases||Diagnostic tests||Physical Examination||Symptoms||Past medical history||Other Findings|
|Na+, K+, Ca2+||CT /MRI||CSF Findings||Gold standard test||Neck stiffness||Motor or Sensory deficit||Papilledema||Bulging fontanelle||Cranial nerves||Headache||Fever||Altered mental status|
|Brain tumour||✔||Cancer cells||MRI||✔||✔||✔||✔||✔||✔||Cachexia, gradual progression of symptoms|
|Delirium tremens||✔||Clinical diagnosis||✔||✔||✔||✔||✔||✔||Alcohol intake, sudden witdrawl or reduction in consumption||Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus,|
|Subarachnoid hemorrhage||✔||Xanthochromia||CT scan without contrast||✔||✔||✔||✔||✔||✔||✔||✔||Trauma/fall||Confusion, dizziness, nausea, vomiting|
|Stroke||✔||Normal||CT scan without contrast||✔||✔||✔||✔||✔||TIAs, hypertension, diabetes mellitus||Speech difficulty, gait abnormality|
|Neurosyphilis||✔||↑ Leukocytes and protein||CSF VDRL-specifc
CSF FTA-Ab -sensitive
|✔||✔||✔||✔||✔||✔||Unprotected sexual intercourse, STIs||Blindness, confusion, depression,
|Viral encephalitis||✔||Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose||Clinical assesment||✔||✔||✔||✔||✔||✔||✔||Tick bite/mosquito bite/ viral prodome for several days||Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioural changes|
|Herpes simplex encephalitis||✔||Clinical assesment||✔||✔||✔||✔||✔||History of hypertension||Delirium, cortical blindness, cerebral edema, seizure|
|Wernicke’s encephalopathy||Normal||✔||✔||✔||History of alcohal abuse||Ophthalmoplegia, confusion|
|CNS abscess||✔||↑ leukocytes >100,000/ul, ↓ glucose and ↑ protien, ↑ red blood cells, lactic acid >500mg||Contrast enhanced MRI is more sensitive and specific,
Histopathological examination of brain tissue
|✔||✔||✔||✔||✔||✔||✔||History of drug abuse, endocarditis, ↓ immune status||High grade fever, fatigue,nausea, vomiting|
|Drug toxicity||✔||✔||Lithium, Sedatives, phenytoin, carbamazepine|
|Conversion disorder||Diagnosis of exclusion||✔||✔||✔||✔||✔||Tremors, blindness, difficulty swallowing|
|Electrolyte disturbance||↓ or ↑||Depends on the cause||✔||✔||Confusion, seizures|
|Febrile convulsion||Not performed in first simple febrile seizures||Clinical diagnosis and EEG||✔||✔||✔||✔||Family history of febrile seizures, viral illness or gastroenteritis||Age > 1 month,|
|Subdural empyema||✔||Clinical assesment and MRI||✔||✔||✔||✔||✔||✔||History of relapses and remissions||Blurry vision, urinary incontinence, fatigue|
|Hypoglycemia||↓ or ↑||Serum blood glucose||✔||✔||✔||History of diabetes||Palpitations, sweating, dizziness, low serum, glucose|
- ↑ Hay, A. D., Redmond, N. and Fletcher, M. Editorial: Antipyretic drugs for children. British Medical Journal, Vol. 333, July 1, 2006, pp. 4-5
- ↑ Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
- ↑ Weston CL, Glantz MJ, Connor JR (2011). "Detection of cancer cells in the cerebrospinal fluid: current methods and future directions". Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
- ↑ Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
- ↑ Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). "Cerebrospinal fluid in cerebral hemorrhage and infarction". Stroke. 6 (6): 638–41. PMID 1198628.
- ↑ Birenbaum D, Bancroft LW, Felsberg GJ (2011). "Imaging in acute stroke". West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
- ↑ DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). "ACR Appropriateness Criteria® on cerebrovascular disease". J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
- ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients". J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
- ↑ Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
- ↑ Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
- Wilkinson, I.M.S. Neurology. Blackwell Science. ISBN 0-86542-854-9
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