Anti-glutamic acid decarboxylase antibody positive neurological syndromes

Abstract

A rare kind of antibody, known as anti-glutamic acid decarboxylase (GAD) autoantibody, is found in some patients. The antibody works against the GAD enzyme, which is essential in the formation of gamma aminobutyric acid (GABA), an inhibitory neurotransmitter found in the brain. Patients found with this antibody present with motor and cognitive problems due to low levels or lack of GABA, because in the absence or low levels of GABA patients exhibit motor and cognitive symptoms. The anti-GAD antibody is found in some neurological syndromes, including stiff-person syndrome, paraneoplastic stiff-person syndrome, Miller Fisher syndrome (MFS), limbic encephalopathy, cerebellar ataxia, eye movement disorders, and epilepsy. Previously, excluding MFS, these conditions were called ‘hyperexcitability disorders’. However, collectively, these syndromes should be known as “anti-GAD positive neurological syndromes.” An important limitation of this study is that the literature is lacking on the subject, and why patients with the above mentioned neurological problems present with different symptoms has not been studied in detail. Therefore, it is recommended that more research is conducted on this subject to obtain a better and deeper understanding of these anti-GAD antibody induced neurological syndromes.

Why It Is Not Always Anxiety: A Tough Diagnosis of Stiff Person Syndrome

“…Low levels of GABA lead to an overall higher firing frequency of nerve cells, which can manifest as either anxiety or even seizure disorders. This may lower the threshold for overactivity of the amygdala, the fear and anxiety center of the brain [ 10 ].…”

Autoimmune Vestibulocerebellar Syndromes

“…12 Classical extraocular movement abnormalities described include positional downbeat or upbeat nystagmus (sitting to supine head hanging position), spontaneous DBN that worsens with lateral gaze, spontaneous or gaze-evoked horizontal nystagmus with or without a rotary component, periodic alternating nystagmus, oscillopsia, opsoclonus, binocular diplopia, internuclear ophthalmoplegia, supranuclear gaze palsies, and eyelid myokymias. 13,14 In general, the presence of opsoclonus is a clue to the opsoclonus-myoclonus syndrome, which is highly indicative of a paraneoplastic or other autoimmune etiology. [15][16][17] The presence and extent of other neurologic signs and symptoms such as cognitive impairment, seizures, psychiatric symptoms, neuropathy, movement abnormalities (e.g., myoclonus, tremors, dystonia), hearing impairment, ocular abnormalities such as uveitis or chorioretinitis, and autonomic features vary across the specific antibody syndromes and are described in detail in the Specific Autoimmune Disorders section.…”

Rare Presentation of a Relapsing Remitting Central Nervous System Vasculitis: A Case Report.

“…Autoimmune encephalitis can manifest with various psychiatric and motor symptoms, which can, in turn, guide evaluation of associated antibody disorders [4]. None of the typical characteristics were present to warrant anti-GAD antibodies [5], or anti-MOG antibodies [6,7], and the MR imaging and rheumatologic serologies point away from the diagnosis [4]. Paraneoplastic panel was also negative.…”