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1.
Figure 6

Figure 6. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Comparison between different KCNA1 mutations. Values of superexcitability (upper panel) and TEd20(peak) (lower panel), for patients with episodic ataxia type 1 grouped by KCNA1 mutation, according to mean superexcitability. Horizontal dashed lines indicate mean values for normal controls.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
2.
Figure 4

Figure 4. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Separation of patients with episodic ataxia type 1 (EA1) from controls (NC) by nerve excitability parameters. (A) Superexcitability; (B) TEd20(peak); (C) TEd40(accom). Dashed horizontal lines are cut-off levels that optimize sensitivity + specificity (see text). Note: data only available for 18 patients in (C).

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
3.
Figure 5

Figure 5. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Separation of patients with episodic ataxia type 1 from controls by two nerve excitability parameters. Open grey circles represent individual values and the dashed ellipse represents the 95% confidence limits for combinations of superexcitability and TEd20(peak) electrotonus values for normal control subjects. Filled circles = patients with episodic ataxia type 1. There is a strong correlation between these two excitability parameters, both of which are highly sensitive to Kv1.1 dysfunction, and all patients with episodic ataxia type 1 were outside the normal limits.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
4.
Figure 1

Figure 1. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Abnormal nerve recovery cycles in episodic ataxia type 1. Threshold changes are percentage increase in threshold current at different times after a supramaximal conditioning stimulus. (A) Superimposed recovery cycles from 30 normal control subjects. (B) Recovery cycles from 20 patients with episodic ataxia type 1. (C) Mean and standard errors of responses in (A and B) superimposed: open grey circles = controls; filled black circles = patients. Small letters indicate parameters referred to in text: a = peak superexcitability; b = peak late subexcitability; c = relative refractory period.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
5.
Figure 2

Figure 2. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Abnormal threshold electrotonus in episodic ataxia type 1. (A) Changes in threshold during and after 100 ms polarizing currents set to +40% and +20%, (depolarizing, top traces), −20% and −40% (hyperpolarizing, bottom traces) of unconditioned threshold current, with decreases in threshold in response to depolarizing current plotted upwards and an increase in response to hyperpolarizing current downwards. Mean and standard errors of controls (grey) and patients with episodic ataxia type 1 (black) plotted as in Fig. 1C. (B) Responses to +40% depolarizing currents expanded. (C) Responses to +20% depolarizing currents. Letters indicate most significantly altered excitability parameters: a = TEd20(peak), i.e. peak threshold reduction during depolarizing current set to 20% of threshold; b = TEh (90–100 ms); c = TEd40(accom), i.e. maximum accommodative increase in threshold after peak, during 40% depolarizing current.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
6.
Figure 3

Figure 3. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Current–threshold (I /V) relationships. (A) Threshold changes 200 ms after the onset of long polarizing currents (x-axis), plotted against polarizing current (y-axis). Filled black circles are means for patients with episodic ataxia type 1 and open grey circles are means of control subjects, plotted with standard errors as in Fig. 1C. (B) Slopes of curves in (A), showing reduction around the resting potential (arrows indicate zero on the x-axis), indicating reduced membrane conductance. (C) Weiss Plot of threshold charge (i.e. threshold current × stimulus duration) against stimulus duration in which the negative intercept on the x-axis (b) represents the strength–duration time constant.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.
7.
Figure 7

Figure 7. From: Nerve excitability studies characterize KV1.1 fast potassium channel dysfunction in patients with episodic ataxia type 1.

Recovery cycle parameters in episodic ataxia type 1 and other nerve pathologies. The cross and ellipse indicate mean and 95% confidence limits of 30 normal control subjects (data from this study). Other symbols indicate mean values for different conditions. Open and filled triangles = four normal nerves depolarized (Depol) and hyperpolarized (Hyperpol) by 1 mA direct current (Kiernan and Bostock, 2001); open and filled diamonds = four normal nerves after 5-min ischaemia (Isch) for 5 min after release of ischaemia (Post-isch) (Kiernan and Bostock, 2001); filled square = six patients with multifocal motor neuropathy (MMN) (Kiernan et al., 2002a); open square = nine patients with chronic renal failure (CRF), before dialysis (Kiernan et al., 2002b); open circle = four patients with tetrodotoxin intoxication from puffer fish ingestion (NC) (Kiernan et al., 2005); filled circle = 20 patients in the present study.

Susan E. Tomlinson, et al. Brain. 2010 December;133(12):3530-3540.

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