EA4
Also known as periodic vestibulocerebellar ataxia, type-4 episodic ataxia (EA4) is an extremely rare form of episodic ataxia differentiated from other forms by onset in the third to sixth generation of life, defective smooth pursuit and gaze-evoked nystagmus. Patients also present with vertigo and ataxia. There are only two known families with EA4, both located in North Carolina. The locus for EA4 is unknown. EA5: CACNB4
There are two known families with type-5 episodic ataxia (EA5).These patients can present with an overlapping phenotype of ataxia and seizures similar to juvenile myoclonic epilepsy. In fact, juvenile myoclonic epilepsy and EA5 are allelic and produce proteins with similar dysfunction.Patients with pure EA5 present with recurrent episodes of ataxia with vertigo. Between attacks they have nystagmus and dysarthria. These patients are responsive to acetazolamide. Both juvenile myoclonic epilepsy and EA5 are a result of mutations in CACNB4, a gene that encodes the calcium channel β4 subunit. This subunit coassembles with α-subunits and produces channels that slowly inactivate after opening.EA5 patients have a cysteine to phenylalanine mutation at position 104.Thus results in channels with 30% greater current than wild-type. As this subunit is expressed in the cerebellum, it is assumed that such increased current results in neuronal hyperexcitability
Coding and noncoding variation of the human calcium-channel beta4-subunit gene CACNB4 in patients with idiopathic generalized epilepsy and episodic ataxia. EA6: SLC1A3
Type-6 episodic ataxia (EA6) is a rare form of episodic ataxia, identified initially in a 10-year-old boy who first presented with 30 minute bouts of decreased muscle tone during infancy.
Periapical periodontitis or apical periodontitis (AP) is an acute or chronic inflammatory lesion around the apex of a tooth root, most commonly caused by bacterial invasion of the pulp of the tooth. It is a likely outcome of untreated dental caries (tooth decay), and in such cases it can be considered a sequela in the natural history of tooth decay, irreversible pulpitis and pulpal necrosis. Other causes can include occlusal trauma due to high spots after restoration work, extrusion from the tooth of root filling material, or bacterial invasion and infection from the gums. Periapical periodontitis may develop into a periapical abscess, where a collection of pus forms at the end of the root, the consequence of spread of infection from the tooth pulp (odontogenic infection), or into a periapical cyst, where an epithelial lined, fluid-filled structure forms. Etymologically, the name refers to inflammation (Latin, -itis) around (peri- ) the root tip or apex (-apical) of the tooth (-odont-). Periradicular periodontitis is an alternative term. Diagnosis
The radiographic features of periapical inflammatory lesions vary depending on the time course of the lesion. Because very early lesions
may not show any radiographic changes, diagnosis of these lesions relies solely on the clinical symptoms. More chronic lesions may show lytic (radiolucent) or sclerotic (radiopaque) changes, or both. Classification
Classification of periapical periodontitis is usually based on whether the process is acute/symptomatic or chronic/asymptomatic. (Note: alternative names for periapical periodontitis include apical periodontitis and periradicular periodontitis.) Acute periapical periodontitis
Acute (or symptomatic) periapical periodontitis....