Author
Etiology
Patients
Site of lesion
Stimulation
Time to surgery
Clinical improvement latency
Evaluation parameters
Responsive n (%)
Kanno et al. (1988) [13]
Trauma/ischemia
10
Cerebral cortex
Cervical SCS
3–6 months
3–14 days
Clinical, EEG, rCBF, dynamic CT, xenon-enhanced CT, catecholamine
9 (90 %)
Matsui et al. (1989) [21]
Trauma/ischemia/tumors
8
Cerebral cortex
Cervical SCS
3–19 months
1–2 months
Clinical
2 (25 %)
Momose et al. (1989) [24]
Trauma/ischemia
1
Cerebral cortex
Cervical SCS
3 months
1 week
PET, 18 FDG, rCBF
1 (100 %)
Kanno et al. (1989) [14]
Trauma/ischemia
6
Diffuse
Cervical SCS
3 months
n.a.
Clinical/CT/ABR/MRI/EEG
4 (66.6 %)
Yokoyama et al. (1990) [38]
Trauma/CVD/hypoxia/tumor
23
Cerebral cortex
Cervical SCS
3–78 months
1–42 months
Clinical, EEG
8 (34.7 %)
Kuwata (1993) [16]
Trauma/vascular/meningitis/tumors
15
Cerebral cortex
Cervical SCS
1–27 months
2 months
EEG, ABR, SEP, neurotrasmitter
4 (26.6 %)
Fujii et al. (1998) [8]
Hypoxia
12
N/A
Cervical SCS
1 month
3 months
MRI, CBF, xenon-enhanced CT, ABR, SEP, clinical
7 (58.3 %)
Liu et al. (2008) [20]
Ischemia
20
Cerebral cortex
Cervical SCS
4.4–95 months
71–287 days
SPECT, neurotransmitter
9 (45 %)
Liu et al. (2009) [19]
Ischemia/trauma
12
Cerebral cortex
Cervical SCS
3–7 months
1–107 days
SPECT, Clinical
6 (50 %)
Kanno et al. (2009) [15]
Ischemia/trauma
201
Diffuse
Cervical SCS
3–12 months
n.a.
Clinical, CT, MRI, SPECT
109 (54.2 %)
Yamamoto et al. (2012) [36]
Trauma/vascular/inflammatory
10
Diffuse
Cervical SCS
3–53 months
6–7 months
Clinical, SPECT
7 (70 %)
Total
318
166 (52.2 %)
Deep Brain Stimulation for CDC
Deep brain stimulation (DBS) is a validated neuromodulation technique traditionally considered to be the “gold standard” for severe cerebral motor symptoms refractory to optimal drug trials. The mechanism of action is the chronic disruption of abnormal neural synchrony between affected brain regions, inhibiting neural activity and moderating abnormal brain function related to disease symptoms [2, 6, 22]. Targets of stimulation have been numerous: some examples are: the subthalamic nucleus for Parkinson’s Disease, the ventralis intermedius (VIM) nucleus of the thalamus for posttraumatic tremor, and the ventroposterolateral nucleus of the thalamus for dystonia. Nowadays, DBS is proposed as a way to alleviate extrapyramidal motor disorders, and research is on-going to explore or validate further indications, such as depression, obsessive compulsive disorder, pain, obesity, anorexia, and epilepsy [4, 6, 18].
In recent years, encouraged by these experiences, the use of DBS has been extended to patients with severe CDC [17]. However, this application entails a number of challenges: the physiopathological mechanisms of CDC involve multiple and often combined events, such as trauma, hemorrhage, ischemia, and anoxia, and so, prospectively, patients liable to benefit from DBS for severe, chronic, or sometimes long-term disorders of consciousness have a wide range of individual phenotypes.
On examining the pertinent literature, we found that a small number of studies explored the effect of DBS in CDC patients (Table 2). A total of 58 CDC patients were treated using DBS from 1968 to 2015; 29 of them (52 %) demonstrated clinical and instrumental signs of arousal from VS. In 1968 McLardy et al. described the first DBS implantation, in a vegetative 19-year-old male, implanted about 8 months after severe head injury. The only reported effects were slight midbrain contacts, such as left orientation of the head and movements of the left hand; slight EEG modifications were also observed [23].
Table 2
DBS in CDC patients
Author | Etiology | Patients | Hemisphere | Electrode location | Time from trauma | Follow-up | Evaluation parameters | Responsive (%) |
---|---|---|---|---|---|---|---|---|
McLardy et al. (1968) [23] | Trauma | 1 | Unilateral left | MRF | 8 m | 1 m | Clinical, EEG | 1 (100 %) |
Hassler et al. (1969) [11] | Trauma | 1 | Bilateral | Anterior thalamus (l), pallidus (r) | n.a. | 5 m | Clinical, EEG | 1 (100 %) |
Sturm et al. (1979) [30] | Vascular | 1 | Bilateral | Lamella medialis (r), nucleus reticularis (l) | 1 m | 1 m | Clinical, EEG | 1 (100 %) |
Tsubokawa et al. (1990) [32] | Trauma,stroke, anoxia | 8 | n.a. | MRF (two cases) CMPf (six cases) | 6 m | 12 m | Clinical, PET, EEG, CBF | 4 (50 %) |
Cohadon and Richer (1984–1993) [5] | Trauma | 25 | Unilateral right | n.a. | 6–15 m | 2 m | Clinical | 13 (52 %)
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