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1                            The hands exhibit dystonic and athetoid posturing and fisting.
2 ) is characterized by attacks of involuntary dystonic and choreoathetoid movements, typically several
3 y correlated with tremor improvement in both dystonic and essential tremor.
4                     Given the improvement in dystonic and hemiballistic movements in these patients a
5 here were no significant differences between dystonics and normals in regional blood flow, blood volu
6 t baseline, experienced as intrusive and ego-dystonic, and associated with higher suspiciousness and
7 hindbrain structures will produce an overtly dystonic animal.
8 eveloped abnormal involuntary movements with dystonic-appearing, self-clasping of limbs, as early as
9 orward rate constant was decreased by 29% in dystonics, as compared with normals (p < 0.05).
10 ay K8644 induced stereotypic tottering mouse dystonic at concentrations significantly below those req
11 etal muscle was normal, appearance of severe dystonic ataxia correlated with postnatal degeneration o
12       Microdialysis of the striatum revealed dystonic attacks in tottering mice to be associated with
13 A) or quinolinic acid (QA) exaggerated their dystonic attacks.
14 l removal of the cerebellum eliminated their dystonic attacks.
15 sed facilitation to inhibition ratios in the dystonic brain.
16 ed a ketogenic diet: one child (who also had dystonic cerebral palsy) was found not breathing at home
17 cipants with a working clinical diagnosis of dystonic cerebral palsy.
18 ontributed substantively to the diagnosis of dystonic cerebral palsy.
19                                   Paroxysmal dystonic choreoathetosis (PDC) is characterized by attac
20                                   Paroxysmal dystonic choreoathetosis (PDC) is characterized by attac
21 ase gene on chromosome 4p; 2) the paroxysmal dystonic choreoathetosis gene at 2q34; 3) the dentatorub
22 orts of dystonia, chorea encephalopathy, and dystonic choreoathetosis occurring as sequelae of strept
23 and the spectrum of NPC component-associated dystonic conditions with localized basal-ganglia abnorma
24  one of the few autosomal dominant inherited dystonic disorders and is caused by mutations in the eps
25 l a central feature to the wider spectrum of dystonic disorders, potentially providing targets for fu
26 le of monogenic variants across the range of dystonic disorders, providing guidance for the introduct
27 ted with many different genetic and acquired dystonic disorders.
28 brief paroxysmal episodes in puberty, either dystonic/dyskinetic or "shivering" attacks, triggered by
29        We defined probabilistic maps of anti-dystonic effects by aggregating individual electrode loc
30                          Following the first dystonic episode, Gnal(+/-) mice in the asymptomatic sta
31 axia, polyspike discharges, and intermittent dystonic episodes.
32 s showed no epileptiform activity during the dystonic events.
33 nical phenotype was novel, with 50% having a dystonic extrapyramidal movement disorder, and 70% a beh
34                                        These dystonic features are the quickest to respond to high fr
35 imates associated with both parkinsonian and dystonic features in a complex, combined movement disord
36 gestion of a stronger tendency for spread of dystonic features in patients with associated tremor.
37                               No animals had dystonic features.
38 regions both symptomatic and asymptomatic to dystonic features.
39 t do not consistently demonstrate subjective dystonic features.
40 ensitive and specific feature distinguishing dystonic from psychogenic torticollis.
41 rols, XDP freezing of gait, and dystonic/non-dystonic gait.
42 ing an asymptomatic motor task involving the dystonic hand and an unrelated asymptomatic task, senten
43 ed primarily cervical dystonia patients with dystonic head tremor and the majority had additional upp
44  mutant mouse (lamb1t) exhibits intermittent dystonic hindlimb movements and postures when awake, and
45 in in cellular function, in either normal or dystonic individuals is not known.
46  cases lacking the GAG deletion (N = 17), in dystonic individuals with apparent homozygosity in the 9
47                                              Dystonic involuntary muscle spasms were specifically ass
48 the importance of this LCI pathology, murine dystonic-like movements are reduced significantly with a
49 on, and link abnormalities of these cells to dystonic-like movements in an overtly symptomatic animal
50 ical model of primary dystonia that exhibits dystonic-like twisting movements has stymied identificat
51 ain cholinergic and GABAergic neurons causes dystonic-like twisting movements that emerge during juve
52                                          The dystonic mice exhibit movement-induced, sustained abnorm
53                      In vivo recordings from dystonic mice revealed abnormal high-frequency bursting
54  link exists between sensory alterations and dystonic motor activity and how mechanisms underlying th
55 interneuron excitation can cause potentially dystonic motor behaviors, we first determined features c
56  al. establish the first animal model with a dystonic motor phenotype and link torsinA hypofunction t
57 type and display vulnerability to developing dystonic movements after systemic or intrastriatal injec
58 acterized by involuntary lightning jerks and dystonic movements and postures alleviated by alcohol.
59 triatum in two different animal models where dystonic movements are thought to originate from abnorma
60 A directly into the striatum ameliorated the dystonic movements but cerebellar microinjections of l-D
61 xplore the hypothesis that the expression of dystonic movements depends on influences from a motor ne
62              They suggest that expression of dystonic movements depends on influences from both basal
63 and a greater understanding of the causes of dystonic movements from the study of genetics, neurophys
64 rmal eye movements were temporally linked to dystonic movements in the limbs on the side opposite the
65                In basal conditions, no overt dystonic movements or postures or change in locomotor ac
66 s characterized by brief episodes of choreic/dystonic movements precipitated by sudden movement.
67 recurrent and brief attacks of choreiform or dystonic movements triggered or exacerbated by sudden vo
68                                         When dystonic movements were triggered by pharmacological sti
69 ity was mainly found in patients with phasic dystonic movements where it was suppressed after high fr
70 ity, axial hypotonia with distal spasticity, dystonic movements, and cerebellar hypoplasia.
71  exhibiting rapid spinal nerve degeneration, dystonic movements, and severe ataxia.
72 R6/2 mouse reveal age-related impairments in dystonic movements, motor performance, grip strength, an
73 ay, central hypotonia, spastic quadriplegia, dystonic movements, rotary nystagmus, and impaired gaze
74 der with a spectrum of symptoms that include dystonic movements, seizures and developmental delay.
75 10 characterized by progressive ataxic gait, dystonic movements, spontaneus seizures, and death by de
76 s to enhance dopamine signalling reduced the dystonic movements, whereas administration of D1- or D2-
77 osing DYT1 gene mutation carriers to develop dystonic movements.
78 pamine, playing a role in the development of dystonic movements.
79 cal condition characterized by myoclonic and dystonic muscle contractions and the absence of other ne
80 ve afferents, such as aberrant feedback from dystonic muscles, may continue to potentiate brainstem c
81                        Stimulated by the ego-dystonic nature of obsessive-compulsive disorder (OCD),
82 lution and a subgroup of patients with a non-dystonic neurodevelopmental phenotype.
83 res from controls, XDP freezing of gait, and dystonic/non-dystonic gait.
84 s, inherited metabolic diseases, and genetic dystonic or parkinsonian syndromes) and are, therefore,
85 system may play a key role in explaining ego-dystonic or self-destructive behaviour.
86                                              Dystonic patients had even less 11-30 Hz power and great
87 nary SPNs of the PD patients compared to the dystonic patients or to the normal levels of striatal ac
88          We report here that when focal hand dystonic patients performed finger-tapping tasks, functi
89 lti-unit signals from the striatum of PD and dystonic patients undergoing deep brain stimulation surg
90 lar histopathological studies on brains from dystonic patients who have undergone DBS.
91 chniques over S1 for therapeutic purposes in dystonic patients.
92     Major reinnervation and/or change in the dystonic pattern occurred following 29% of the procedure
93 ified that loss of striatal KCTD5 leads to a dystonic phenotype, coordination deficits, and skewed tr
94 n the short disease duration and predominant dystonic phenotype, these results are well in line with
95  splicing of 10% of Scn8amedJ pre-mRNA and a dystonic phenotype.
96 effect, producing viable adults with a novel dystonic phenotype.
97 rked improvement, and 4 (0.03%) no effect on dystonic posture.
98  be a consequence of maintaining an abnormal dystonic posture.
99  variant SMS (n = 2, limited to 1 limb [with dystonic posture] or back), and progressive encephalomye
100 s of mice elicited reliable and reproducible dystonic postures of the trunk and limbs.
101 and impaired gait that rapidly progressed to dystonic postures.
102 rence of early and late oral automatisms and dystonic posturing of an upper extremity was analysed se
103                                              Dystonic posturing was also associated with higher defor
104 rainstem nuclei involved in arousal and that dystonic posturing would be associated with high forces
105 l events including loss of consciousness and dystonic posturing.
106 HOPSANDs), which are mainly characterized by dystonic presentations.
107 he process can be described as an example of dystonic proton coupled electron transfer.
108         Clinical outcomes were faciobrachial dystonic seizure (FBDS) resolution, modified Rankin Scal
109 d a distinctive adult-onset, frequent, brief dystonic seizure semiology that predominantly affected t
110 GI1-IgG-positive patients with faciobrachial-dystonic seizures (9 of 39, 31%).
111 seizure semiologies, including faciobrachial dystonic seizures (FBDS), in addition to the amnesia.
112 ptoms, and seizures, including faciobrachial dystonic seizures (FBDS).
113           We have termed these faciobrachial dystonic seizures (FBDS).
114 nly male (35%, p=0.004), while faciobrachial dystonic seizures (FBDS; 65%, p=0.047) and hyponatraemia
115 d immunotherapy to treat their faciobrachial dystonic seizures (P = 0.02).
116 s with limbic encephalitis and faciobrachial dystonic seizures associated with LGI1 antibodies.
117                 In conclusion, faciobrachial dystonic seizures can be prospectively identified as a f
118 ient, but a longer duration of faciobrachial dystonic seizures correlated with a reduction of pallidu
119 he four cases with relapses of faciobrachial dystonic seizures during corticosteroid withdrawal.
120                                Faciobrachial dystonic seizures have recently been reported as immunot
121 hly associated and distinctive faciobrachial dystonic seizures is very important.
122  encephalitis and additionally faciobrachial dystonic seizures may occur.
123 veloped hyponatremia; none had faciobrachial dystonic seizures or malignancy.
124 nalities are striking and only faciobrachial dystonic seizures reliably differentiate these two condi
125                                Faciobrachial dystonic seizures were controlled more effectively with
126                                Faciobrachial dystonic seizures were unnoticed in four (17%) of 24 pat
127 the first prospective study of faciobrachial dystonic seizures with serial assessments of seizure fre
128 s associated with cessation of faciobrachial dystonic seizures within 1 week in three and within 2 mo
129 at (ii) effective treatment of faciobrachial dystonic seizures would accelerate recovery and prevent
130       We hypothesized that (i) faciobrachial dystonic seizures would show a differential response to
131 % for patients presenting with faciobrachial dystonic seizures, 63% for NMDAR-IgG encephalitis and 48
132 viour disorder, nine (38%) had faciobrachial dystonic seizures, and seven (29%) had focal onset seizu
133 ents with limbic encephalitis, faciobrachial dystonic seizures, Morvan's syndrome and neuromyotonia.
134                                Faciobrachial dystonic seizures, possibly pathognomonic for the VGKCC
135 escribed epileptic syndrome of faciobrachial dystonic seizures.
136 nt disorder characterized by sudden onset of dystonic spasms and slow movements.
137 atric changes, viral prodrome, faciobrachial dystonic spells or facial dyskinesias, and mesial tempor
138 d environmental factors that can trigger the dystonic state.
139                  Cross-correlograms from the dystonic subjects revealed a central peak with a median
140                                              Dystonic subjects showed bilateral abnormalities of perc
141    In experiments without vibratory stimuli, dystonic subjects showed normal movement of the tracking
142 l perception of motion, but not position, in dystonic subjects.
143 tudes in theta and beta bands correlate with dystonic symptom severity across patients.
144                                              Dystonic symptom severity significantly correlated with
145  coupling showed an inverse correlation with dystonic symptom severity.
146 sorder characterized by myoclonic jerks with dystonic symptoms and caused by mutations in paternally
147 ternal pallidum are robustly associated with dystonic symptoms in cervical dystonia and may be a usef
148 zepine, and trihexyphenidyl, which alleviate dystonic symptoms in patients.
149 served in patients with head tremor, whereas dystonic symptoms involving the arms were more frequentl
150                                              Dystonic symptoms involving the neck were more frequentl
151 latory connectivity and its association with dystonic symptoms provides further confirmation of cereb
152 present the neurons directly associated with dystonic symptoms, impaired release of neurotransmitters
153 ficantly with either severity or duration of dystonic symptoms.
154  training may reverse sensory impairment and dystonic symptoms.
155 splay an unusually large phenotypic range of dystonic symptoms.
156 ation of oxotremorine to these mice triggers dystonic symptoms.
157  cerebello-thalamic excitability and reduced dystonic symptoms.
158 retraining and stimulation for restoring the dystonic symptoms.
159 ulated genes and 61 of them were involved in dystonic syndrome-related pathways, like synaptic transm
160                         To date, at least 13 dystonic syndromes have been distinguished on a genetic
161  same time, the phenotypes of other forms of dystonic syndromes have been expanded or linked together
162                                          The dystonic syndromes include a large group of diseases tha
163                                Patients with dystonic syndromes sometimes develop increasingly freque
164 ndscape with respect to the cause of various dystonic syndromes that is likely to make a direct impac
165 hat link DYT6 to other primary and secondary dystonic syndromes.
166    Two sisters had early-onset parkinsonism (dystonic toe curling, action tremor, masked face, bradyk
167            The pathophysiology of idiopathic dystonic torticollis is unclear and there is no simple t
168  corticoreticular and corticospinal drive in dystonic torticollis.
169 d efficacious treatments for upper-extremity dystonic tremor (DT).
170 t feature that differs substantially between dystonic tremor and essential tremor and should be furth
171 d force tremor during the grip-force task in dystonic tremor and essential tremor cohorts.
172 abnormal functional connectivity networks in dystonic tremor and essential tremor groups relative to
173 rk-level activation and connectivity between dystonic tremor and essential tremor patient cohorts to
174                       The pathophysiology of dystonic tremor and essential tremor remains partially u
175                                Patients with dystonic tremor and essential tremor were characterized
176  connectivity z-scores were able to classify dystonic tremor and essential tremor with 89% area under
177 rget for patients with medication-refractory dystonic tremor and essential tremor, respectively.
178 activation and connectivity in patients with dystonic tremor and essential tremor.
179 or due to Parkinson's disease, essential and dystonic tremor and tremor related to multiple sclerosis
180       At the same time, clinical features of dystonic tremor can resemble that of essential tremor an
181  the effects were far more widespread in the dystonic tremor group as changes in functional connectiv
182                                          The dystonic tremor group included primarily cervical dyston
183  ventral intermediate nucleus region and for dystonic tremor in the ventralis oralis posterior nucleu
184                         A unique pattern for dystonic tremor included widespread reductions in functi
185 thesis that the pathophysiology underpinning dystonic tremor involves both the cerebello-thalamo-cort
186                                              Dystonic tremor is presumably under-reported, and we aim
187                                              Dystonic tremor is under-reported and this underscores t
188       In patients with medication-refractory dystonic tremor or essential tremor, deep brain stimulat
189 ospective case note analysis did not suggest dystonic tremor or indeterminate tremor in any of them.
190 imal targets for DBS in essential tremor and dystonic tremor using a combination of volumes of tissue
191 urke-Fahn-Marsden Dystonia Rating Scale) and dystonic tremor were examined.
192                 We included 20 patients with dystonic tremor who underwent unilateral thalamic DBS, a
193  currently proposed clinical subdivision of 'dystonic tremor' and 'tremor associated with dystonia'.
194 otor regions in essential tremor, whereas in dystonic tremor, the correlation was tighter with the pr
195 gnatures that relate to clinical features of dystonic tremor.
196 y correlated with tremor improvement only in dystonic tremor.
197 been cases of indeterminate senile tremor or dystonic tremor.
198 r LD (n = 199 [78.0%]), followed by adductor dystonic voice tremor (n = 26 [10.2%]) and ETVT (n = 13

 
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