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anti - glutamic acid decarboxylase antibody ( gad - ab)-associated cerebellar ataxia is a rare neurological disorder characterized by cerebellar symptoms concomitant with high gad - ab levels in serum and cerebrospinal fluid ( csf ) .
we report on 2 female siblings ( aged 74 and 76 years ) presenting with gradual progression of rotational vertigo , gait ataxia and vertical diplopia , continuously progressing for 6 months and 6 years , respectively .
their medical histories revealed late - onset type 1 diabetes mellitus ( t1 dm ) and other concomitant autoimmune disorders ( grave 's disease , hashimoto 's thyroiditis ) .
the diagnosis of gad - ab - associated cerebellar ataxia with particular brainstem involvement was established in both women .
after the exclusion of an underlying malignancy , immunosuppressive therapy has been initiated in both patients , which resulted in stabilization in one and in clinical improvement in the other patient .
the unique association of autoantibody - mediated cerebellar ataxia and late - onset t1 dm in 2 siblings with similar clinical and paraclinical phenotypes strengthens the concept that hereditary factors might play a relevant role also in autoimmune diseases so far considered to be sporadic .
moreover , the occurrence of continuous vertical diplopia broadens the clinical spectrum of gad - ab - associated neurological syndromes .
anti - glutamic acid decarboxylase antibody ( gad - ab)-associated cerebellar ataxia is a rare , but increasingly detected , autoimmune neurological disorder characterized by the clinical presence of a cerebellar syndrome concomitant with high gad - ab levels in serum and cerebrospinal fluid ( csf ) [ 1 , 2 , 3 ] .
recent studies have linked gad - ab cerebellar ataxia with type 1 diabetes mellitus ( t1 dm ) , other autoimmune endocrine disorders and , occasionally , even with paraneoplastic etiologies .
although a positive family history of other autoimmune diseases such as t1 dm and thyroiditis is common in gad - ab cerebellar patients , previous studies did not determine a familial predisposition of gad - ab cerebellar ataxia itself , which is thus considered to be sporadic .
the here described occurrence of gad - ab cerebellar ataxia in 2 female siblings suggests that an underlying immunogenetical mechanism might additionally account for disease incidence and individual susceptibility .
a 74-year - old caucasian woman ( patient 1 ) with no significant medical history presented with constant rotational vertigo , progressive gait ataxia with a tendency to fall to the right side and vertical diplopia increasing in right gaze .
her elder sister , a 76-year - old caucasian woman ( patient 2 ) likewise presented with a 6-year - history of rotational vertigo , continuous gait ataxia and marked vertical diplopia .
symptoms were reported to have presented subacutely at onset and had initially been misdiagnosed as brainstem infarction . in both patients ,
neurological examination revealed remarkably similar symptoms including gaze - evoked nystagmus and a slight abduction deficit of the right eye as well as ataxia and dysmetria in the upper and lower extremities with right - sided predominance . because of the pronounced gait ataxia of both patients , they depended on a wheeled walker . upon motor , reflex and sensory examination ,
no relevant findings were elicited , in particular no signs of dysarthria , peripheral neuropathy , spasticity , areflexia , vegetative symptoms or fasciculations that could have pointed to one of the hereditary ataxias , such as sca1 , 2 , 3 and 6 .
cerebral mri findings showed mild generalized atrophy and multiple white matter lesions in both patients ( fig .
d ) . except for glycated hemoglobin ( hba1c ) levels , which were expectably elevated due to the existing t1 dm ,
comprehensive workup with extended autoimmune laboratory examinations revealed remarkably high serum and csf gad - ab levels in both siblings ( fig .
other autoantibodies were negative , in particular antibodies against the nmda , ampa or gaba(b ) receptor , lgi1 , caspr2 , mag , glycin receptor , or onconeuronal antibodies .
further csf analysis showed slight pleocytosis in patient 1 and oligoclonal immunoglobulin bands in both patients .
in addition , the medical history of patient 1 revealed hashimoto 's thyroiditis with elevated serum antithyroid peroxidase antibody levels and recently diagnosed t1 dm , whereas patient 2 exhibited a 7-year - history of grave 's disease with high levels of thyroid - stimulating immunoglobulins and a 6-year - history of insulin - dependent t1 dm ( table 1 ) .
their family history revealed a 73-year - old brother suffering from rheumatism and another 75-year - old brother without relevant diseases .
the diagnosis of cerebellar ataxia with gad - abs was established in both siblings based on the subacute onset , csf inflammation in patient 1 , the very high gad - ab titers , the partial response to immunotherapy , the age at onset and the typical constellation of insulin - dependent diabetes .
since the detection of gad - abs can occasionally indicate a paraneoplastic etiology [ 2 , 5 ] , we undertook full - body computed tomography scans in both patients as well as whole - body and brain positron emission tomography in patient 1 , all of which showed no pathological findings , suggesting the absence of any malignancy .
plasma separation by immunoadsorption was used to eliminate pathogenic antibodies from the serum compartment by binding to the extracorporeal columns . for this ,
patient 1 received 5 cycles every other day which led to subtle improvement of gait ataxia .
extended treatment with a further 10 cycles of immunoadsorption eventually resulted in remarkable improvement of gait which allowed the patient to walk without her walking frame . in patient 2 , 7 cycles of plasmapheresis were administered every other day and resulted in subjective improvement of gait disability , and a slightly diminished degree of gaze - evoked nystagmus was seen on follow - up examination .
however , relevant impairment persisted so that immunosuppressive therapy was escalated in both women to 1,000 mg rituximab intravenously according to common practice .
both patients gave their written informed consent for data analysis and the publication of this case report .
in this familial case report , we present the occurrence of autoimmune gad - ab - associated cerebellar ataxia in 2 female siblings with resembling clinical phenotype concomitant with t1 dm starting at a comparatively high age . the pattern of gad - ab - related autoimmune central nervous system ( cns ) disorders is characterized by heterogeneous and occasionally overlapping clinical syndromes , including the stiff person syndrome , cerebellar ataxia , progressive encephalomyelitis with rigidity and myoclonus , limbic encephalitis , epilepsy and paraneoplastic syndromes [ 2 , 5 , 6 ] .
these cns disorders often occur in association with other autoimmune diseases , mainly t1 dm .
although the presence of gad - abs is equally characteristic for both , > 100-fold higher levels of gad - abs in serum are frequently seen in neurological disorders compared to t1 dm . moreover , intrathecal synthesis   and a different epitope specificity of gad - abs   have been reported in neurological syndromes . whereas the immunogenetical relationship of t1 dm with specific human leukocyte antigen genes is widely known and well established in the literature , data on immunogenetical features of gad - ab - associated neurological disorders are scarce , likely due to the comparatively low incidence and the lack of reports on familial cases
. a markedly higher frequency of gad - ab - seropositive cases was found in first - degree relatives of t1 dm patients compared to healthy controls [ 9 , 10 ] .
however , decisive inferences concerning a possible familial predisposition of gad - ab neurological disorders can not be drawn , since the causative mechanisms of requisitely high serum and csf gad - ab levels still remain unclear . in our reported cases ,
both women exhibited typical cerebellar symptoms , i.e. continuous rotational vertigo , progressive gait ataxia and gaze - evoked nystagmus with subacute onset , detection of csf oligoclonal bands and concomitant autoimmune diseases , implicating the diagnosis of gad - ab cerebellar ataxia [ 1 , 4 ] .
the additional occurrence of persistent vertical diplopia , as described in both cases , is an uncommon finding .
although versatile symptoms including multifocal brainstem involvement have been reported in some patients , to our knowledge , the literature provides only 1 specific case of gad - ab cerebellar ataxia with additional vertical diplopia , in which double vision lasted for only 10 days as an early prodromal symptom which had already disappeared before the eventual development of the full cerebellar syndrome . in our cases ,
constant vertical diplopia was present at symptom onset and has been persisting throughout the entire disease course , implicating that diplopia can be added to the clinical features of gad - ab cerebellar ataxia , broadening the known clinical spectrum [ 1 , 3 , 4 , 11 ] .
interestingly , both related patients exhibited an identical phenotype even with regard to age at first symptoms , type of onset and csf oligoclonal bands instead of developing 2 different neurological syndromes within the broad gad - ab - associated spectrum .
this might be related to the excessively high titers of gad - abs that have been particularly linked to cerebellar ataxia in contrast to the stiff person syndrome [ 1 , 6 ] .
the fact that high titers are required for clear cns symptoms underscores the pathogenic role of gad - abs in cerebellar damage , potentially due to enzyme inhibition of intracytoplasmic gad or antibody - induced suppression of gaba release [ 1 , 7 , 12 ] .
the clinical improvement in patient 1 further supports this concept , even though a definite causal relationship between gad - ab autoimmunity and ataxia can not be provided .
this limitation is known in the field and has been attributed mainly to the presence of additional mechanisms , such as further antibodies against surface antigens   or pathogenic cytotoxic t cells .
the finding of gad - abs in the 2 siblings suggests a hereditary component of gad - ab cerebellar ataxia .
however , this is rather unlikely as gad - ab cerebellar ataxia is considered a rare disease that occurs only sporadically .
therefore , our case presentation suggests immunogenetical mechanisms possibly leading to a familial predisposition to develop autoimmune gad - ab - associated neurological disorders . against the background of the diagnostic challenge , especially regarding the group of late - onset cerebellar ataxias , our case presentation gives rise to the question as to whether a positive family history for the disease allows the ruling in or ruling out of a hereditary , sporadic or autoimmune disorder in the respective individual diagnosis . taken together , by describing the unique association of late - onset autoantibody - mediated ataxia and diabetes in 2 siblings , the cases
strengthen the concept that hereditary factors might play a relevant role also in diseases thought to be primarily sporadic .
moreover , the occurrence of multifocal cerebellar and brainstem symptoms in both patients broadens the established clinical spectrum of gad - ab - associated neurological syndromes .
nevertheless , further research is necessary to eventually understand the full scope of autoimmunity in gad - ab - associated disorders , their relationship to other autoimmune diseases and their respective immuno- and pathogenetic mechanisms .
backgroundanti - glutamic acid decarboxylase antibody ( gad - ab)-associated cerebellar ataxia is a rare neurological disorder characterized by cerebellar symptoms concomitant with high gad - ab levels in serum and cerebrospinal fluid ( csf).case reportwe report on 2 female siblings ( aged 74 and 76 years ) presenting with gradual progression of rotational vertigo , gait ataxia and vertical diplopia , continuously progressing for 6 months and 6 years , respectively . 
 autoimmune laboratory examinations showed remarkably increased serum and csf gad - ab levels . 
 their medical histories revealed late - onset type 1 diabetes mellitus ( t1 dm ) and other concomitant autoimmune disorders ( grave 's disease , hashimoto 's thyroiditis ) . 
 cerebral mri and laboratory examinations were unremarkable . 
 the diagnosis of gad - ab - associated cerebellar ataxia with particular brainstem involvement was established in both women . after the exclusion of an underlying malignancy 
 , immunosuppressive therapy has been initiated in both patients , which resulted in stabilization in one and in clinical improvement in the other patient.discussionthe unique association of autoantibody - mediated cerebellar ataxia and late - onset t1 dm in 2 siblings with similar clinical and paraclinical phenotypes strengthens the concept that hereditary factors might play a relevant role also in autoimmune diseases so far considered to be sporadic . 
 moreover , the occurrence of continuous vertical diplopia broadens the clinical spectrum of gad - ab - associated neurological syndromes .