Deep brain stimulation can be applied under sedation for surgery in the treatment of patients with essential tremor. It is not known exactly why the effect on the GABA system and locus cereous responses can occur against different therapeutic agents in these patients.

75 years old, male, without any co-existing disease, with essential tremor patient, planned deep brain stimulation operation under sedoanalgesia, one week before the operation the patient evaluated. There wasn’t found any cardiovascular or respiratory and endocrine system disease on physical examination and past medical history. Brain magnetic resonance imaging was planned under sedoanalgesia in the MR unit. We planned to perform sedation with propofol fractional doses of 20 mg than when he has reached the Ramsey 3 - 4 levels, maintained the propofol infusion 0.5 - 1 mg/kg/hour. His initial blood pressure was 110 - 60 mmHg, health rate 60 beat/hour. We made a standard monitorisation and administered two time 20 mg propofol dose within 3 minute interval and maintained dose at 0.5 mg/kg/min. After 40th minute the patient fully sedated and became ramsey 4 and was began to snoring. The pulse oximeter values reduced at 92% - 90% - 89% continuously. We placed an airway and increased the SpO2 level 93%. On 20th minute the patient blood pressure suddenly dropped 50/35 mmHg and we stopped the propofol. Efedrin was given and blood pressure was achieved to the basal levels immediately. After 1 week we tried to brain magnetic resonance imaging and I gave the half dose of which was given the first time. Everything was ok and we finished the procedure and we recommend to the surgent and neurologist that must make a sleeping pattern analysis for obstructive sleep apne or sleeping disorders for this patient. On the DBS day we decided to perform procedure with dexmedetomidine. We were administered the loading dose and maintained dose. The patient’s initial bispectral index values 98% - 99% (BIS aspect). After 20 minute neither BIS values, nor Ramsey changes. We started to give very high doses dexmedetomidine but it didn’t worked so we decided to turn propofol on 30th minute again and after the administration of the 10 mg propofol, BIS values was 85% - 88% throughout the operation. We gave 40 - 50 mg propofol totally throughout the procedure and Ramsey Sedation Scale went on level 3 - 4. At the end of the operation the patient was transferred to the neurosurgery service that fully awake, cooperate, with spontaneous breathing, cardiovascular and hemodynamic stabilization and without neurologic complication.

Essential tremor is unknown exactly: which is a neurodegenerative disease group treated with Gamma-Aminobutyric acid (GABA) receptor agonists, antiepileptic drugs, gabapentin, benzodiazepines and deep brain stimulation techniques. Sedative agents can be used during deep brain stimulation (DBS) placement procedures. Despite of both propofol and dexmedetomidine providing the same clinically result, when we evaluated the electroencephalographic (EEG) changes, we saw almost the similar activity suppression pattern of this two different drugs. Propofol is an agonist on Gamma-Aminobutyric acid (GABA) receptors and dexmedetomidine is an alfa 2 adrenoreceptor agonists [1] .

We explained the dexmedetomidine unresponsiveness first with his sleeping disorders, because he has got severe sleeping disorder (confirmed with sleep lab) and reported severe neuronal damage in locus coeruleus region in this group of patients. Also dexmedetomidine affects locus coeruleus. But the second question is that the cause of this exaggerated responses of the brain for the propofol in this patient. And we started the search on this fact. It seems that propofol decreases the connectivity especially thalamus, but it also increases the connectivity within the pons of the brainstem during propofol-induced mild sedation [2] [3] . The second view point shown by Yağar and his colleagues. They investigate the association between the effect of alfa 2A-Adrenergic Receptor (ADRA2A) C-1291G gene polymorphism and clinical effects of dexmedetomidine on one hundred and ten patients undergoing coronary artery surgery. They showed that there was a weak effect of ADRA2A C1291G gene polymorphism in response to dexmedetomidine [4] . Alfa 2A-Adrenergic Receptor (ADRA2A) gene is highly polymorphic [5] . G allele carriers were more sedated than others with dexmedetomidine [4] . Propofol coordinated frontal EEG alpha oscillations and asynchronous thalamocortical slow oscillations similar to the dexmedetomidine showed slow oscillations and dex spindles called’ spindle like activity’. However, in terms of behavioral and clinical characteristics of these two drugs, it shows different characteristics [6] [7] .

When performed functional MRI imaging in healthy people under propofol sedation which reduces activity in the pons, thalamus and brain stem has been shown to increase the activity. That seems to be the key component of a break in the thalamocortical communication during propofol sedation [8] [9] .

The roads leading from the thalamus to the cortex are formed by major GABAergic inhibitory effects. Positron emission tomography studies done to suggest that propofol is associated with a decrease in neuronal activity in the thalamus of the anesthetic-induced unconsciousness [10] . Propofol showed sedation at low doses, at high doses constitute unconsciousness. Dexmedetomidineis create nonREM like sleep in a short-term period of slow oscillation. Propofol is while creating a similar pattern is observed in more prolonged OFF periods [11] .

GABA hypothesis in essential tremor patients have been proposed. GABAergic system is especially located on the cerebellum. This hypothesis leading to the loss of cerebellar Purkinje cells in cerebellar neuron degeneration low GABA system activity, disinhibition of pacemaker activity of cerebellar neurons, increased activity of thalamus and rhythmic activity of thalamocortical circuit that leads tremor [12] .

A slight increase in CSF and serum concentrations of glutamate in a study by way of example, reduced levels of GABA, glycine and serine low levels have been identified. It also strengthened the argument that patients with ET have GABAergic dysfunction [13] .

Positron Emission Tomographic scans which have done with [C¹¹] flumazenil on ET patients, showed that there was a lateral premotor cortex abnormality on venterolateral thalamus in the GABA_A receptor binding region. GABA_A receptor binding abnormally increased in cerebellar―thalamic input path was also determined [14] .

In our case, we observed very low dose (40 mg of propofol, 2.5 hours operation time) despite the effective tremor control and adequate level of sedation (Ramsey 3 - 4, BIS values 80% - 92%) (Figure 1) was provided on the one hand

supports of GABAergic hypothesis, increased binding to GABA_A receptor in response to propofol.

Yorulmazi, I.S., Esbah, A.U., Dikici, S., Ozlu, O. and Er, U. (2017) Unanswered Response to Dexmede- tomidine and Exaggerated Response to Propofol during Deep Brain Stimulation in Essential Tremor Case. Open Access Library Journal, 4: e3605. https://doi.org/10.4236/oalib.1103605