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Acoustic neuroma (schwannoma)
Adult brain tumors
Pediatric brain tumors
Transient ischemic attack
Cavernous sinus thrombosis
Spinocerebellar ataxia (NORD)
Tethered spinal cord syndrome
Lewy body dementia
Normal pressure hydrocephalus
Acute disseminated encephalomyelitis
Central pontine myelinolysis
JC virus (Progressive multifocal leukoencephalopathy)
Cavernous sinus thrombosis
Idiopathic intracranial hypertension
Opsoclonus myoclonus syndrome (NORD)
Restless legs syndrome
Early infantile epileptic encephalopathy (NORD)
Cauda equina syndrome
Treponema pallidum (Syphilis)
Vitamin B12 deficiency
Concussion and traumatic brain injury
Spinal muscular atrophy
Carpal tunnel syndrome
Thoracic outlet syndrome
Lambert-Eaton myasthenic syndrome
Adult brain tumors: Pathology review
Central nervous system infections: Pathology review
Cerebral vascular disease: Pathology review
Congenital neurological disorders: Pathology review
Dementia: Pathology review
Demyelinating disorders: Pathology review
Headaches: Pathology review
Movement disorders: Pathology review
Neurocutaneous disorders: Pathology review
Neuromuscular junction disorders: Pathology review
Pediatric brain tumors: Pathology review
Seizures: Pathology review
Spinal cord disorders: Pathology review
Traumatic brain injury: Pathology review
0 / 40 complete
0 / 10 complete
drug therapy for p. 565
treatment p. 726
absence seizures p. 726
Epilepsy means “seizure disorder”, so people with epilepsy have recurring and unpredictable seizures. A seizure is a period where cells in the brain, or neurons, are synchronously active, or active at the same time, when they’re not supposed to be.
Now when I say that neurons are “active”, I mean that they’re firing or sending a message using electrical signals relayed from neuron to neuron.
And if you look at a neuron under a microscope, each electrical signal that passes through it is really just ions flowing in and out of it through protein channels.
The way this ion flow is controlled is through neurotransmitters, a type of signaling molecule, and receptors. Neurotransmitters bind to the receptors and basically tell the cell to either open up the ion channels and relay the electrical message, called excitatory neurotransmitters, or close the ion channels and stop the electrical message, called inhibitory neurotransmitters.
During a seizure, clusters of neurons in the brain become temporarily impaired and start sending out a ton of excitatory signals, over and over again, and these are sometimes said to be paroxysmal.
These paroxysmal electrical discharges are thought to happen due to either too much excitation, or too little inhibition (which are kinda two sides of the same coin, right?).
The main excitatory neurotransmitter in the brain is glutamate, and NMDA is the primary receptor that responds to glutamate by opening ion channels that let calcium in, a positive ion that tells the cell to send signals.
Some patients with epilepsy seem to have fast or long-lasting activation of these receptors. On the flip side, the main inhibitory neurotransmitter in the brain is GABA, which binds to GABA receptors that tell the cell to inhibit the signal by opening channels that let in chloride ions, which are negative ions that tell the cell to inhibit signals.
Some patients with epilepsy seem to have genetic mutations in which their GABA receptors are dysfunctional, and so they aren’t able to help inhibit signals.
In addition to potentially having a primary genetic cause, though, these receptors and ion channels might be affected by all sorts of things like brain tumors, brain injury or infection.
Whether it’s a decrease in inhibition or an increase in activation, when groups of neurons start firing simultaneously, over and over, it’s often noticed by others as obvious outward signs, like jerking, moving, and losing consciousness, but can also be subjective experiences that are only noticed by the person experiencing it, like fears or strange smells, it all depends on which neurons in the brain are affected.
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