from Chronic Diseases of Consciousness: State of the Art in Neuromodulation for Persistent Vegetative State and Minimally Conscious State


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 %)


CDC chronic diseases of consciousness, SCS spinal cord stimulation, EEG electroencephalogram, SPECT single-photon emission computed tomography, PET positron emission tomography, rCBF regional cerebral blood flow, CBF cerebral blood flow, ABR auditory brainstem response, n.a. not available, CVD cardiovascular disease, SEP somatosensory evoked potential, FDG fluoro deoxy glucose, MRI magnetic resonance imaging





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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Jun 24, 2017 | Posted by in NEUROSURGERY | Comments Off on from Chronic Diseases of Consciousness: State of the Art in Neuromodulation for Persistent Vegetative State and Minimally Conscious State

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