FDG-PET in Creutzfeldt-Jakob disease: Analysis of clinical-PET correlation

Figures & data

TABLE 1. Patient characteristics, codon 129 polymorphism, presence of periodic sharp wave complexes on electroencephalogram and CSF 14-3-3 protein, associated clinical signs/syndromes, time between symptom onset and PET, and lateralization of PET hypometabolism.

Patient nr	Sex	Age	codon 129	PSWC	14-3-3	Ataxia	Visual	Pyramidal	Myoclonus	Apraxia	Dystonia	Sensory	Parkinsonism	CBS	Time onset-PET (days)	Lateralisation of PET hypometabolism
1	F	54	Met/Met	+	+	Y	Y	Y	N	Y	N	N	N	N	75	L
2	M	86	Met/Met	+	+	N	N	N	Y	N	Y	N	N	N	66	L
3	F	52	Met/Met	+	+	Y	N	N	N	Y	Y	N	N	Y	77	L
4	F	60	Met/Met	+	+	Y	N	N	N	N	Y	N	Y	Y	135	L
5	F	70	Val/Val	−	+	Y	N	N	N	Y	N	N	N	N	53	L
6	F	60	Met/Val	−	+	Y	Y	N	N	N	N	N	N	N	247	L
7	F	79	NP	+	+	N	N	N	N	N	N	N	N	N	37	R
8	F	65	Met/Met	+	+	Y	Y	Y	Y	N	Y	Y	N	Y	28	L
9	F	75	Met/Met	+	+	N	N	N	N	Y	N	N	Y	Y	126	L
10	M	63	Met/Met	+	+	N	N	N	N	Y	N	N	N	N	27	L
11	M	79	NP	+	+	N	Y	Y	Y	Y	Y	N	Y	Y	18	R
12	M	69	Val/Val	−	+	Y	N	N	N	Y	N	N	N	N	105	R
13	F	57	Val/Val	−	+	Y	Y	Y	Y	N	N	N	Y	N	126	L
14	M	79	Met/Met	+	+	N	N	N	N	Y	Y	N	N	Y	51	L
15	F	70	Met/Met	+	+	Y	Y	Y	Y	N	Y	Y	N	Y	41	L

CBS, corticobasal syndrome; Met, methionine; Val, valine; NP, not performed; Y, yes; N, no; L, left; R, right; PSWC, periodic sharp wave complexes.

TABLE 2. FDG-PET data for the entire (global) CJD group and the different clinical CJD subgroups.

CJD-control analysis; inter-CJD analysis (* is added when hypometabolic brain areas corresponded to the clinical signs)
	Global	Cerebellar ataxia	Visual signs	Pyramidal signs	Myoclonus	Limb apraxia	Limb dystonia	Sensory loss	Parkinsonism	Corticobasal syndrome
orbitofrontal cortex									left>right
mesial frontal cortex						bilateral
lateral frontal cortex	left	left	left	left	left	left left	left		left	left
lateral prerolandic frontal cortex							left*			left*
frontal subcortical lobe		right	right
lateral parietal cortex					left left*	left left*	left left*			left left*
mesial parietal cortex	left>right	left>right	left	left	left>right	bilateral	left		left>right	left left
mesial temporal cortex		left
lateral posterior temporal cortex	left	left	right		left				left	left left
lateral temporal-occipital cortex							left
mesial occipital cortex						left
occipital cortex			left right≥left *			left
subcortical occipital lobe				left
anterior deep grey matter			left
pons		bilateral *
middle cerebellar peduncles		left≥right*

FIGURE 1. SPM showing decreased FDG-PET metabolism (using a stringent level of significance of p<0.001 and an extent threshold of 100 voxels) in the left lateral frontal cortex and the left mesial parietal cortex, and to a lesser degree the right mesial parietal cortex left lateral posterior temporal cortex in CJD patients in comparison to controls.

FIGURE 2. Inter-CJD SPM analysis, using a stringent level of significance of p<0.001 and an extent threshold of 100 voxels, in patients with cerebellar ataxia, showing FDG-PET hypometabolism in the pons, the bilateral (left-predominant) middle cerebellar peduncles, the right frontal subcortical lobe, and the left mesial temporal cortex.

FIGURE 3. Inter-CJD SPM analysis showing decreased metabolism (using a stringent level of significance of p<0.001 and an extent threshold of 100 voxels) in the bilateral (right-predomiant) occipital cortex and the right frontal subcortical lobe in CJD patients with visual signs.

FIGURE 4. Inter-CJD SPM analysis (using a stringent level of significance of p<0.001 and an extent threshold of 100 voxels), in CJD patients with myoclonus, showing hypometabolism in the left lateral parietal cortex.

FIGURE 5. Inter-CJD SPM analysis, in the CJD patients with limb dystonia, showing left lateral parietal cortex and left lateral prerolandic frontal cortex hypometabolism (using a stringent level of significance of p<0.001 and an extent threshold of 100 voxels).

FIGURE 6. Inter-CJD SPM analysis showing hypometabolism in the left lateral prerolandic frontal cortex, the left -lateral more than mesial- parietal cortex, and the left lateral posterior temporal cortex in patients with corticobasal syndrome.