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creutzfeldt - jakob disease ( cjd ) is a rare progressive neurodegenerative disease affecting one person per million per year .
prion diseases are caused by abnormal metabolism and conformation of the cellular prion protein , the primary function of which is ambiguous .
cjd is characterized by rapidly progressive dementia , ataxia , myoclonus and by pyramidal and extrapyramidal motor symptoms .
definite diagnosis of cjd requires histopathological examination of the brain tissue usually obtained post - mortem .
however , clinical symptoms , typical eeg - findings , detection of 14 - 3 - 3 protein in the cerebrospinal fluid ( csf ) and abnormal cortical and subcortical signal in diffusion - weighted mri allow clinical diagnosis of cjd .
typical eeg in cjd displays frontal intermittent rhythmical delta activity ( firda ) and periodic sharp wave complexes ( pswc ) .
firda is usually detected already in the early stages of the disease whereas pswcs suggest a more progressed disease .
the appearance of motor symptoms , particularly myoclonus , usually correlates with the appearance of pswcs in eeg [ 3 , 4 ] . in two cjd patients , the source locations of pswcs correlated with the extent of visible lesions in diffusion - weighted mri .
a 33-year - old man developed a progressive memory dysfunction and impaired fine motor skills during a one - year period .
regular use of alcohol was reported , but otherwise the patient had had no major health problems . in the initial clinical examination , the patient had significant amnesia and ataxia .
the symptoms were considered to be alcohol - related , thiamine substitution was started and the patient was referred to the district hospital for rehabilitation . due to progressive cognitive decline , ataxia , vertical gaze palsy and gait abnormality , the patient was again referred to the university hospital .
abnormal diffusion - weighted signals in the basal ganglia , thalami and frontotemporal cortex , more prominent in the left hemisphere , were detected in the control mri ( fig .
the initial mri also showed bilateral signal abnormalities in the basal ganglia in t2-weighted and flair sequences . increased tau protein and 14 - 3 - 3 protein in csf supported the diagnosis of cjd . in an eeg recorded on the same day , but not simultaneously with meg , slow wave activity was more pronounced in the left hemisphere , but no sharp wave complexes were detected .
occasional myoclonus , triggered by sudden loud noises , was observed one week before the meg recording .
the patient died from a probable pulmonary embolism six days after the meg recording , before planned follow - up meg .
the meg was recorded in a magnetically shielded room with a 306-sensor elekta whole - head meg system ( elekta oy , helsinki , finland ) .
meg signals were sampled at 600 hz and band - pass filtered at 0.1 - 200 hz .
auditory evoked fields ( aefs ) were elicited by 1-khz , 50-ms tones ( 1.5 - 2.5 s random isi ) , delivered via a panel loudspeaker attached to the wall of the shielded room .
the signals were post - processed with the tsss ( elekta maxfilter ; elekta oy ) artifact rejection software .
the spontaneous meg data were inspected visually and sharp transients were selected for equivalent current dipole ( ecd ) analysis .
sources of slow oscillations ( 0.1 - 8 hz ) were localized using an experimental beamformer package ( elekta oy ) .
the noise power , required for covariance statistics , was calculated from high - pass filtered data thus labeling oscillations that had frequency greater than 8 hz as noise .
a ten - second segment with the clearest firda - like activity was selected for the analysis .
epochs contaminated by eye movements and blinks in eog were discarded from the averages ; 150 epochs were included in the averaged aefs .
all source localization was done using an individual single - layer boundary element method model obtained using the freesurfer and the mne - suite software ( athinoula a. martinos center for biomedical imaging , massachusetts general hospital , boston , mass .
a 33-year - old man developed a progressive memory dysfunction and impaired fine motor skills during a one - year period .
regular use of alcohol was reported , but otherwise the patient had had no major health problems . in the initial clinical examination , the patient had significant amnesia and ataxia .
the symptoms were considered to be alcohol - related , thiamine substitution was started and the patient was referred to the district hospital for rehabilitation . due to progressive cognitive decline , ataxia , vertical gaze palsy and gait abnormality , the patient was again referred to the university hospital .
abnormal diffusion - weighted signals in the basal ganglia , thalami and frontotemporal cortex , more prominent in the left hemisphere , were detected in the control mri ( fig .
the initial mri also showed bilateral signal abnormalities in the basal ganglia in t2-weighted and flair sequences . increased tau protein and 14 - 3 - 3 protein in csf supported the diagnosis of cjd . in an eeg recorded on the same day , but not simultaneously with meg , slow wave activity was more pronounced in the left hemisphere , but no sharp wave complexes were detected .
occasional myoclonus , triggered by sudden loud noises , was observed one week before the meg recording .
the patient died from a probable pulmonary embolism six days after the meg recording , before planned follow - up meg .
the meg was recorded in a magnetically shielded room with a 306-sensor elekta whole - head meg system ( elekta oy , helsinki , finland ) .
meg signals were sampled at 600 hz and band - pass filtered at 0.1 - 200 hz .
auditory evoked fields ( aefs ) were elicited by 1-khz , 50-ms tones ( 1.5 - 2.5 s random isi ) , delivered via a panel loudspeaker attached to the wall of the shielded room .
the signals were post - processed with the tsss ( elekta maxfilter ; elekta oy ) artifact rejection software .
the spontaneous meg data were inspected visually and sharp transients were selected for equivalent current dipole ( ecd ) analysis .
sources of slow oscillations ( 0.1 - 8 hz ) were localized using an experimental beamformer package ( elekta oy ) .
the noise power , required for covariance statistics , was calculated from high - pass filtered data thus labeling oscillations that had frequency greater than 8 hz as noise .
a ten - second segment with the clearest firda - like activity was selected for the analysis .
epochs contaminated by eye movements and blinks in eog were discarded from the averages ; 150 epochs were included in the averaged aefs .
all source localization was done using an individual single - layer boundary element method model obtained using the freesurfer and the mne - suite software ( athinoula a. martinos center for biomedical imaging , massachusetts general hospital , boston , mass .
firda - like intermittent runs of high amplitude slow wave activity were observed as well .
the sources of low frequency oscillations were scattered over a relatively large area , but the maximum activity in the beamformer results occurred in the left frontotemporal area , in line with the visual impression of the meg signals ( fig .
however , the clearest cluster of ecd sources was found in the left frontotemporal region ( fig .
auditory stimulation produced clearly identifiable p50 m , n100 m and p200 m deflections in both hemispheres .
the p50 m and p200 m had a somewhat larger amplitude in the left than in the right hemisphere .
ecd sources were approximately in the normal anatomical locations in close vicinity of the sylvian fissure ( fig .
the ratio of the p200m / n100 m source amplitudes was 1.7 in the left and 0.6 in the right hemisphere .
our patient was quite young and had thalamic hyperintensity in mri raising suspicion of variant cjd .
in addition , the patient had no signs of depression and apathy at the onset of symptoms that are typical for variant cjd .
the clinical diagnosis of cjd is challenging as the symptoms , the results from imaging studies and the csf findings are somewhat nonspecific .
the typical pswcs in eeg are only present in some patients and usually signify the terminal state of cjd . further , in some cases , the typical eeg findings disappear with disease progression .
meg revealed abnormal slow wave activity that was more prominent in the more damaged left hemisphere , as shown by mri .
the sharp transients were clearly multifocal , but their sources were also concentrated in the left hemisphere .
thus , two different source localization methods ( ecds and beamformer ) produced results that were consistent with the left - dominant cortical and subcortical abnormalities in the diffusion - weighted mri .
previous eeg studies have shown either normal   or deteriorated   brainstem auditory evoked potentials in cjd .
the sources of aef p50 m and p200 m deflections were stronger in the left , more damaged hemisphere . in healthy subjects , the ratio of p200m / n100 m deflections is about 0.3 . in our patient ,
the ratio of p200m / n100 m source strengths was 1.7 in the left and 0.6 in the right hemisphere , suggesting abnormally dominant p200 m deflections particularly in the more affected left hemisphere .
in contrast , there appears to be excitation or disinhibition of the p50 m and p200 m generators .
our study shows that it is possible to obtain good quality meg recordings from a patient with cjd , and model the sources of the abnormal signals .
the distribution of the sources of the abnormal waveforms suggest an extensive disorder of cortical function in cjd .
disinhibition or abnormal excitation , as suggested by the aefs , may be a factor contributing to myoclonia triggered by sudden loud noises in cjd .
obviously , a single case study is inadequate to determine whether meg source modeling offers any benefit over the standard eeg as a diagnostic tool . to answer this question ,
creutzfeldt - jakob disease ( cjd ) is a rare neurodegenerative disease with no effective therapy available . 
 we recorded spontaneous magnetoencephalography and auditory evoked fields ( aefs ) from a male patient with a rapidly progressive memory disorder , ataxia and myoclonus . 
 post - mortem examination confirmed sporadic cjd . 
 sources of the abnormal slow wave activity were localized with a beamformer software . 
 sources of sharp transients and aefs were modeled with equivalent current dipoles . 
 the estimated sources of spontaneous activity abnormalities were more dominant in the left hemisphere , in line with left - dominant abnormalities in diffusion - weighted mri . 
 sources of aefs were found in both temporal lobes . 
 magnetoencephalography measurements on cjd patients are feasible , and provide efficient means for localizing abnormal cortical activity in cjd .