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\title{Evoked Potentials in the Prognosis of Surgical Treatment of Cerebellar Syndrome in Chiari Malformation Type 1}
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             \author[1]{Rano  Ismailova}

             \author[2]{Gayrat  Kariev}

             \author[3]{Qurbonova  R.R.}

             \affil[1]{  Andijan State Medical Institute,}

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\date{\small \em Received: 1 January 1970 Accepted: 1 January 1970 Published: 1 January 1970}

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\begin{abstract}
        


The scientific work presents the results of a neurophysiological examination of 63 patients with cerebellar symptoms in Chiari malformation of type I according to MRI data. All patients underwent a multimodal protocol including BAEP, SSEP and ENMG examination. Neurophysiological criteria of the cerebellar syndrome in type 1 Chiari malformation have been identified, which in a comparative analysis are the most informative in decision making regarding conservative or surgical treatment.

\end{abstract}


\keywords{chiari malformation type 1, tonsils ectopia, cerebellar syndrome, brainstem auditory evoked potential (BAEP).}

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\section[{Introduction}]{Introduction}\par
eurological disorders in case of anomalies of the craniovertebral junction are extremely diverse and consist of both clinical signs of brainstem compression by lowered cerebellar tonsils and liquorodynamic disorders \hyperref[b0]{[1,}\hyperref[b3]{3,}\hyperref[b7]{7]}.\par
Analysis of the dynamics of neurological disorders does not always provide objective information, and a more informative functional quantitative scale for assessing neurological symptoms, proposed by Egorov et al., 2002 \hyperref[b3]{[3]} determines the dynamics of neurological disorders in the pre-and postoperative period in Arnold Chiari type I (AK type I). A more objective picture of the functional state of the structures of the craniovertebral transition is provided by a comparison of clinical and neurophysiological research data \hyperref[b6]{[6,}\hyperref[b7]{7,} {\ref 10]} Unfortunately, there is still no single system for assessing the degree of functional deficiency in this pathology. At the same time, the high proportion of subjective neurological disorders makes it difficult to determine the degree of compensation of the disease \hyperref[b4]{[4,}\hyperref[b9]{9,} {\ref 10]}. The question -to observe or to operate? -is extremely important in the modern practice of neurologists and neurosurgeons. Modern neurophysiological diagnostic methods make it possible to absolutely accurately objectify the level of pathological disorders and determine the degree of functional involvement of certain anatomical structures. Clinical manifestations of Chiari type I anomaly are described in detail in the literature. Many authors identify from 3 to 6 variants of clinical syndromes \hyperref[b3]{[3,}\hyperref[b4]{4,}\hyperref[b7]{7,} {\ref 10]}. Most often, cerebellar, bulbar, pyramidal and syringomyelia variants are distinguished, and almost all researchers of this pathology point to a high proportion of patients with cerebellar disorders in AK type I \hyperref[b8]{[8,} {\ref 10]}. Comparative analysis of subjective, objective symptoms in AK type I and neurophysiological data of ASEP, SSEP and ENMG in various AK type I syndromes greatly facilitates the decision on the issue of conservative and surgical tactics, however, a small amount of information about such results in the literature determined the purpose of our study.\par
The purpose of the study is to determine the dependence of the formation of the cerebellar syndrome on the degree of ectopia of the cerebellar tonsils and to identify significant predictors according to evoked potentials in determining conservative or surgical tactics in patients with this syndrome in Chiari type 1 anomaly. 
\section[{II.}]{II.} 
\section[{Materials and Methods}]{Materials and Methods}\par
We studied 207 patients with AK type I who were treated at the Republican Specialized Scientific-Practical Medical Centre of Neurosurgery from 2015 to 2018, aged 18 to 57 years, the number of men was 82 observations, and women were 125 observations. Among them, 63 patients were identified with neurological disorders characteristic of the cerebellar syndrome in AK type I. All patients were divided into groups depending on the degree of displacement of the cerebellar tonsils below the Chamberlain line. The first group consisted of 17 patients with ectopia of 0-5 mm, the second had 75 patients with ectopia of 5-10 mm, the third was 84 patients with ectopia of 10-15 mm, in the fourth group consisted of 31 patients with the displacement and ectopia was more than 15 mm according to MRI study. The control group consisted of 30 healthy individuals.\par
The standard for determining the degree of descent of the cerebellar tonsil in Chiari anomalies was the Chamberlain line, passing from the hard palate to the Opistion (a point located in the centre of the posterior edge of the BSO) \hyperref[b2]{[2,}\hyperref[b8]{8,}\hyperref[b9]{9]}. We considered the displacement of the cerebellar tonsils beyond the Chamberlain line up to 5 mm to be acceptable. In our studies, we used the Chamberlain line to guide the anatomical anomalies of the craniovertebral junction and the degree of cerebellar tonsil ectopia (Fig.  {\ref 1}).\par
Fig.  {\ref 1}: MRI patient S., 29 years old with an anomaly of the craniovertebral junction with a displacement of the cerebellar tonsils below the Chamberlain line up to 7 mm on both sides with clinical manifestations of cerebellar syndrome.\par
All patients underwent a multimodal neurophysiological protocol, including acoustic stem evoked potentials (ASEPs), somatosensory evoked potentials (SSEPs), and motor evoked potentials (ENMG) \hyperref[b7]{[7]}. The studies were carried out on a 4channel Synapsis complex (Neurotech, Russia) with computer data processing.\par
For ASEP, the standard vertex-mastoid lead (M1-Cz, M2-Cz) was used.\par
During SSEP, the electrodes were installed according to the standard C4-Fz method -with stimulation of n.medianus S C3-Fz-with stimulation of n.medianus D. Stimulation was carried out with electrical impulses in the projection of the median nerve at the level of the wrist with a current of 15-20 mA, a frequency of 2 Hz.\par
Stimulation EMG was performed for n.glossopharyngeus with the establishment of recording electrodes in accordance with muscle innervation. If necessary, we supplemented the studied nerves based on the neurological deficit.\par
Statistical data analysis was carried out using IBM SPSS Statistics 26 version. Differences in the distribution of quantitative values were assessed using Student's parametric test. To assess the likelihood of surgical treatment, the method of discriminant analysis was used, followed by the construction of a prognostic function, and an assessment of the specificity and sensitivity of the model. Statistically significant differences in the group of operated and non-operated patients were assessed using the Wilks coefficient ?. 
\section[{III.}]{III.} 
\section[{Results and Discussion}]{Results and Discussion}\par
Patients with cerebellar disorders had the highest representation among the examined patients -63 cases (30.4\%).\par
After analyzing the above complex of subjective and objective neurological symptoms in patients with type I Chiari anomaly, we identified 4 types of clinical syndromes -cerebellar, bulbar, pyramidal, syringomyelitic, which were most clearly formed in groups of patients. The distribution of these syndromes in patients with AK type I, depending on the degree of displacement of the cerebellar tonsils below the Chamberlain line, is proposed in Table \hyperref[tab_0]{1} (Fig. \hyperref[fig_0]{2}).  As can be seen from the presented data, cerebellar syndrome with clinical symptoms of dizziness, tinnitus, various types of nystagmus, static and dynamic ataxia phenomena most often occurred in patients of the ? and ? groups with tonsil descent to 5-9 mm and accounted for more than half of the cases (58.8\% and 52.0\% respectively). The representation of cerebellar syndrome in patients of the ? and ? groups was significantly less. So, with severe tonsil ectopia of 10-15 mm, the cerebellar syndrome was observed in 12 (14.3\%) patients, and in the group with ectopia of more than 15 mm, it was observed in only 2 examined individuals. Such a low number of patients in the ? and ? groups with manifestations of the cerebellar syndrome, in our opinion, is associated with the intactness of the cerebellar pathways with a pronounced displacement of the cerebellar tonsils.\par
Next, we analyzed data from neurophysiological studies in patients with Chiari 1 anomaly. The data obtained from ASEP studies in patients with cerebellar syndrome are presented in Table \hyperref[tab_1]{2}. It was found that in all examined patients, the latent periods of peaks ? and ? were extended bilaterally with significant differences compared to healthy individuals. The average values of the latencies of the remaining components -?, ?, ? were unchanged compared to the results of the control group. The amplitude indices of the ? and ? peaks were significantly increased relative to the control values, which dissociated from the general idea of depression of the amplitude indices in ASEP in patients with pathology of stem structures. In our opinion, an increase in the amplitudes of the ? components in patients with cerebellar syndrome indicated functional irritation of the stem structures at the level of the upper olivary complex. An analysis of the average values of the interpeak intervals showed a slight delay in ?-? and ?-? in the examined group with significant differences with control individuals, which indicated a slowdown in conduction at the pontomesencephalic level. Peak-to-peak intervals ?-? were preserved compared to the control group, which can be explained by the intactness of the peripheral portion of the auditory analyzer. Fig.  {\ref 3}: An example of ASEP in a patient with clinical manifestations of cerebellar syndrome is presented. There is an increase in the amplitude of the P? peak bilaterally with a relative expansion of the peak-to-peak interval P?-P? We analyzed the data of somatosensory EPs in 63 patients with clinical manifestations of cerebellar AK type I syndrome. Registration of SSEP was performed during stimulation of the median and tibial nerves from 2 sides, the average SSEP values were compared with the values in the control group. The results of the SSEP study in cerebellar syndrome are presented in Table \hyperref[tab_2]{3}. As can be seen from the above data, in the group of patients with cerebellar syndrome, there was a significantly significant increase in the latency of the N13 component up to 14.5 ms compared with the control group, which was more often symmetrical bilateral (84\% of cases). The amplitude indicators of all SSEP components were preserved relative to healthy individuals. The expansion of the N13-N20 interpeak intervals up to 6.9 ms was isolated in the group of patients with cerebellar AK type I; the parameters of the N9-N13 and N9-N20 interpeak intervals were unchanged compared to the control values.\par
When analyzing the data on SSEP indicators for stimulation of the tibial nerve, shown in Table \hyperref[tab_3]{4}, a significant extension of the latent period of the N30 component to 38.1 ms was determined in patients with cerebellar syndrome relative to the control group. Changes in the amplitudes of the components N22, N30, P37 in the study group of patients were not recorded. The N30-P37 peak-to-peak interval was moderately extended to 12.5 ms in the majority of cases (68\%) with cerebellar syndrome compared to healthy individuals, the N22-N30, N22-P37 peak-to-peak latencies were consistent with the control group. Thus, the analysis of SSEP data during stimulation of the median and tibial nerves revealed an increase in the latency of the N13, N30 components in patients with cerebellar AK type 1 syndrome in the predominant number of cases combined with an expansion of the interpeak intervals N13-N20 (64\% of patients) and N30-P37 (55\% of patients ), which indicated a slowdown in afferentation at the level of the cervical spinal cord and then the medulla oblongatathe thalamus cortex with a tendency to reduce postsynaptic activation of the nuclei of the medulla oblongata.\par
We analyzed the ENMG data obtained by stimulation of the oculomotor, facial, glossopharyngeal nerves, as well as the median and tibial nerves in a group of patients with cerebellar disorders in AK type 1. As follows from Table \hyperref[tab_4]{5} below, motor conduction velocity SPI eff was slightly reduced in the facial and glossopharyngeal nerves with significant differences from the control group. In the oculomotor nerve, the efferent velocity in the study group was preserved relative to the control. The parameters of the conduction velocity of the SPI eff impulse along the nerves of the upper and lower extremities were unchanged in comparison with healthy individuals. Also, we did not register significant deviations in the Amax values of the M-response amplitudes for all the studied nerves in the group of patients. However, after stimulation, in 27\% of patients with cerebellar syndrome, pathological waves along the facial nerve were noted, while in the group of healthy individuals such a phenomenon was not recorded. In our opinion, small downward deviations of the SPI eff values in the facial and glossopharyngeal nerves against the background of relatively intact values of the M-response amplitudes indicated the functional involvement of the structures of the pons and medulla oblongata in cerebellar syndrome. Pathological waves along the facial nerve may have corresponded to irritative disorders at the cerebellopontine level. Unchanged parameters of SPI eff and amplitudes of muscle responses during stimulation of the median and tibial nerves in the group of patients with AK type 1 indicated the absence of dysfunction of the segmental apparatus in cerebellar disorders.\par
Taking into account the above data, we tried to use the discriminant analysis method to identify the likelihood of an operative outcome of treatment in patients with neurological manifestations of the cerebellar syndrome in AK type 1, depending on the degree of tonsil ectopia, as well as quantitative indicators -the amplitudes and latencies of the components of evoked potentials -ASEP, SSEP and ENMG, followed by the construction of a predictive model.\par
As a result of discriminant analysis by the method of stepwise selection, the following model was obtained (1):Y oper =-8,328+0,302*? ect +1,667*? ?3-?5 ,\textbf{(1)}\par
where Y oper is a discriminant function that characterizes the likelihood of surgery in patients with cerebellar syndrome with AK type 1, X act is the degree of tonsil ectopia (mm), ? ?3-?5 is the latency of the inter-peak interval ?3-?5 in ASVP. The discrimination constant separating patients into operated and non-operated was determined as the value of the function equidistant from the centroids, which amounted to 1.259 in the group of operated patients, and 2.698 in the group of non-operated patients.\par
The discrimination constant for this model was calculated by the formula -arithmetic mean of centroids (sum/2), or KD=(1,259-2,698)/2=-0,719 when comparing the mean values of the discriminant function in both groups of operated and non-operated patients with AK type 1 using the Wilks coefficient ?, statistically significant differences were established (p=0.0001).\par
Given the calculated values of the prognostic discriminant function, it is possible to determine a high or low probability of the risk of surgical intervention in patients with cerebellar syndrome with Chiari anomaly type 1: with a function value of more than -0.719, the patient belonged to the group with a high probability of surgical intervention, and with a function value of less than -0.719 The risk of surgery was significantly lower.\par
The sensitivity of the model was 88.2\%, the specificity was 100.0\%.\par
Thus, as a result of discriminant analysis, we obtained a function that allows us to predict the likelihood of a surgical outcome of treatment in patients with cerebellar syndrome in AK type 1.\par
In conclusion, it should be noted that the proposed prognostic model of a conservative or surgical outcome of the disease in patients with AK type 1 has a significant relationship with the degree of cerebellar tonsil ectopia and changes in neurophysiological parameters according to evoked potentials. At the same time, registration of the expansion of interpeak latencies P3 and P5 according to the ASEP study is especially important in addressing the issue of surgical intervention in patients with manifestations of cerebellar syndrome in AK type 1.\begin{figure}[htbp]
\noindent\textbf{2}\includegraphics[]{image-2.png}
\caption{\label{fig_0}Fig. 2 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{}\includegraphics[]{image-3.png}
\caption{\label{figure3}}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{1} \par 
\begin{longtable}{P{0.2217391304347826\textwidth}P{0.026877470355731223\textwidth}P{0.10750988142292489\textwidth}P{0.0974308300395257\textwidth}P{0.07055335968379448\textwidth}P{0.10750988142292489\textwidth}P{0.06383399209486165\textwidth}P{0.09071146245059288\textwidth}P{0.06383399209486165\textwidth}}
\tabcellsep \tabcellsep ? group\tabcellsep \multicolumn{2}{l}{? group}\tabcellsep \multicolumn{2}{l}{? group}\tabcellsep \multicolumn{2}{l}{? group}\\
\tabcellsep \tabcellsep 0-4 mm\tabcellsep \multicolumn{2}{l}{5-9 mm}\tabcellsep \multicolumn{2}{l}{10-15 mm}\tabcellsep \multicolumn{2}{l}{>15 mm}\\
\tabcellsep \tabcellsep (n=17)\tabcellsep (n=75)\tabcellsep \tabcellsep (n=84)\tabcellsep \tabcellsep (n=31)\tabcellsep \\
Syndromes\tabcellsep \#\tabcellsep \%\tabcellsep \#\tabcellsep \%\tabcellsep \#\tabcellsep \%\tabcellsep \#\tabcellsep \%\\
Cerebellar\tabcellsep 10\tabcellsep 58.8\tabcellsep 39\tabcellsep 52.0\tabcellsep 12\tabcellsep 14.3\tabcellsep 2\tabcellsep 6.45\\
Bulbar\tabcellsep -\tabcellsep -\tabcellsep 10\tabcellsep 13.3\tabcellsep 20\tabcellsep 23.8\tabcellsep 9\tabcellsep 29.0\\
Pyramidal\tabcellsep -\tabcellsep -\tabcellsep 5\tabcellsep 6.67\tabcellsep 21\tabcellsep 25.0\tabcellsep 1\tabcellsep 3.23\\
Syringomyelitic\tabcellsep -\tabcellsep -\tabcellsep 18\tabcellsep 24.0\tabcellsep 31\tabcellsep 36.9\tabcellsep 19\tabcellsep 61.3\\
Without syndromes\tabcellsep 7\tabcellsep 41.2\tabcellsep 3\tabcellsep 4.0\tabcellsep -\tabcellsep -\tabcellsep -\tabcellsep -\end{longtable} \par
 
\caption{\label{tab_0}Table 1 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{2} \par 
\begin{longtable}{P{0.3105575326215895\textwidth}P{0.06755634638196915\textwidth}P{0.04234875444839858\textwidth}P{0.09780545670225385\textwidth}P{0.14721233689205218\textwidth}P{0.04436536180308422\textwidth}P{0.14015421115065244\textwidth}}
\multicolumn{2}{l}{Latent period, ms}\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\multicolumn{2}{l}{Control group (n=30)}\tabcellsep ??\tabcellsep ??\tabcellsep ??\tabcellsep ??\tabcellsep ??\\
S\tabcellsep \multicolumn{2}{l}{1.79± 0.16}\tabcellsep 2.95 ± 0.18\tabcellsep 3.94 ± 0.24\tabcellsep 5.06 ± 0.22\tabcellsep 5.97 ±0.25\\
D\tabcellsep \multicolumn{2}{l}{1.72 ± 0.17}\tabcellsep 2.98 ± 0.19\tabcellsep 3.92 ± 0.22\tabcellsep 5.13 ± 0.20\tabcellsep 6.02± 0.25\\
Cerebellar\tabcellsep syndrome\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
(n=63)\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
S\tabcellsep \multicolumn{2}{l}{1.74 ± 0.18}\tabcellsep 2.96 ± 0.17\tabcellsep 4.25 ± 0.25\tabcellsep 5.25± 0.21\tabcellsep 6.55± 0.22*\\
D\tabcellsep \multicolumn{2}{l}{1.68 ± 0.16}\tabcellsep 3.02 ± 0.19\tabcellsep 4.25 ± 0.21*\tabcellsep 5.38± 0.19\tabcellsep 6.70 ±0.24*\\
\multicolumn{2}{l}{Amplitude, µV}\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\multicolumn{2}{l}{Control group (n=30)}\tabcellsep \tabcellsep ??\tabcellsep ??\tabcellsep \tabcellsep ??\\
\tabcellsep S\tabcellsep \tabcellsep 0.286± 0.05\tabcellsep \multicolumn{2}{l}{0.262± 0.04}\tabcellsep 0.368 ±0.06\\
\tabcellsep D\tabcellsep \tabcellsep 0.282± 0.04\tabcellsep \multicolumn{2}{l}{0.265± 0.06}\tabcellsep 0.338± 0.08\\
\multicolumn{2}{l}{Cerebellar syndrome (n=63)}\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\tabcellsep S\tabcellsep \tabcellsep 0.348± 0.03\tabcellsep \multicolumn{2}{l}{0.370± 0.03**}\tabcellsep 0.375 ± 0.05*\\
\tabcellsep D\tabcellsep \tabcellsep 0.340± 0.04\tabcellsep \multicolumn{2}{l}{0.372± 0.05**}\tabcellsep 0.380 ± 0.07*\\
\multicolumn{2}{l}{Peak intervals, ms}\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\multicolumn{2}{l}{Control group (n=30)}\tabcellsep \tabcellsep ??-??\tabcellsep ??-??\tabcellsep \tabcellsep ??-??\\
\tabcellsep S\tabcellsep \multicolumn{2}{l}{2.19± 0.16}\tabcellsep 2.06± 0.18\tabcellsep \tabcellsep 4.38± 0.22\\
\tabcellsep D\tabcellsep \multicolumn{2}{l}{2.24± 0.18}\tabcellsep 2.08± 0.22\tabcellsep \tabcellsep 4.46± 0.24\\
Cerebellar\tabcellsep syndrome\tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
(n=63)\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\tabcellsep S\tabcellsep \multicolumn{2}{l}{2.56± 0.15}\tabcellsep 2.52± 0.14**\tabcellsep \tabcellsep 4.90±0.21*\\
\tabcellsep D\tabcellsep \multicolumn{2}{l}{2.88± 0.17}\tabcellsep 2.60± 0.18**\tabcellsep \tabcellsep 4.82±0.20*\\
\multicolumn{7}{l}{Significant differences in identical indicators between the control group and the group of patients (Student t-test) *-?? 0.05, **-? ?}\\
0.01\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_1}Table 2 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{3} \par 
\begin{longtable}{P{0.2850931677018634\textwidth}P{0.2639751552795031\textwidth}P{0.30093167701863355\textwidth}}
Latency, ms\tabcellsep Control group (n=30)\tabcellsep Cerebellar Syndrome (n=63)\\
N9 Erb\tabcellsep 9.6±0.7\tabcellsep 9.4±0.7\\
N13 Neck\tabcellsep 13.2±0.8\tabcellsep 14.5±0.7*\\
N20 Cortex\tabcellsep 18.8±1.0\tabcellsep 18.9±1.2\\
Amplitude, µV\tabcellsep \tabcellsep \\
N9 Erb\tabcellsep 5.4±2.5\tabcellsep 5.6±2.2\end{longtable} \par
 
\caption{\label{tab_2}Table 3 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{4} \par 
\begin{longtable}{P{0.4925925925925926\textwidth}P{0.17037037037037037\textwidth}P{0.18703703703703703\textwidth}}
Latency, ms\tabcellsep Control group (n=30)\tabcellsep Cerebellar Syndrome (n=63)\\
N22 lumbar\tabcellsep 23.6±1.9\tabcellsep 23.2±1.6\\
N30 cervical\tabcellsep 30.6±2.5\tabcellsep 38.1±1.2**\\
?37 Cortex\tabcellsep 37.5±3.4\tabcellsep 36.±3.0\\
Amplitude, µV\tabcellsep \tabcellsep \\
N22 lumbar\tabcellsep 1.3±0.5\tabcellsep 1.7±0.3*\\
N 30 cervical\tabcellsep 0.9±0.3\tabcellsep 1.1±0.2\\
?37 Cortex\tabcellsep 2.6±1.5\tabcellsep 2.9±1.5\\
Peak intervals, ms\tabcellsep \tabcellsep \\
N22-N30\tabcellsep 7.62±1.14\tabcellsep 7.86±1.07\\
N30-?37\tabcellsep 8.05±1.32\tabcellsep 12.5±1.54*\\
N22-?37\tabcellsep 15.7±1.65\tabcellsep 16.9±1.35\\
\multicolumn{3}{l}{Significant differences in identical indicators between the control group and the group of patients (Student t-test) *-?? 0.05, **-? ?}\\
0.01\tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_3}Table 4 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{5} \par 
\begin{longtable}{P{0.49335664335664337\textwidth}P{0.14265734265734267\textwidth}P{0.16197552447552446\textwidth}P{0.05201048951048951\textwidth}}
Control group (n=30)\tabcellsep SPI eff, m/s\tabcellsep Amax, µV\tabcellsep Additional pathological waves\\
Oculomotor nerve\tabcellsep 29.4±2.2\tabcellsep 1080±105.5\tabcellsep -\\
Facial nerve\tabcellsep 39.5±1.8\tabcellsep 1235±126.3\tabcellsep -\\
Glossopharyngeal nerve\tabcellsep 42.6±2.0\tabcellsep 1860±164.0\tabcellsep -\\
Median nerve\tabcellsep 61.0±1.7\tabcellsep 6254±267.0\tabcellsep -\\
Tibial nerve\tabcellsep 49.6±2.1\tabcellsep 7125±745.5\tabcellsep -\\
Cerebellar Syndrome (n=63)\tabcellsep \tabcellsep \tabcellsep \\
Oculomotor nerve\tabcellsep 29.1±2.0\tabcellsep 1072±105.8\tabcellsep \\
Facial nerve\tabcellsep 34.8±1.6**\tabcellsep 1130±138.0*\tabcellsep +\\
Glossopharyngeal nerve\tabcellsep 39.2±1.4**\tabcellsep 1851±170.5\tabcellsep \\
Median nerve\tabcellsep 60.4±1.5\tabcellsep 6158±245.6\tabcellsep \\
Tibial nerve\tabcellsep 48.3±1.9\tabcellsep 7245±760.8\tabcellsep \\
\multicolumn{4}{l}{Significant differences in identical indicators between the control group and the group of patients (Student t-test) *-?? 0.05, **-? ?}\\
0.01\tabcellsep \tabcellsep \tabcellsep \end{longtable} \par
 
\caption{\label{tab_4}Table 5 :}\end{figure}
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\end{document}
