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Epilepsia partialis continua associated with nonketotic hyperglycemia Clinical and biochemical profile of 21 patients.

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Epilepsia Partiah Continua Associated
with Nonketotic Hyperglycemia: Clinical
and Biochemical Profile of 21 Patients
Brij M. Singh, MD, and R o b e r t J. Strobos, M D
I n 2 1 patients, epilepsia partialis continua (EPC) was an early symptom of nonketotic hyperglycemia and occurred
during an initial phase of hyponatremia and mild hyperosmolality. EPC persisted for an average of 8 days, and its
duration correlated predominantly with the degree of hyponatremia. Depression of consciousness and cessation of
seizures occurred with increasing severity of hyperglycemia and hyperosmolality. I n 9 patients, EPC was the first
symptom leading to the diagnosis of diabetes mellitus. Four patients died of serious associated illness.
T h e majority of the patients had evidence of a localized structural cerebral lesion. Metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of EPC in areas of focal cerebral damage.
Singh BM, Strobos RJ: Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and
biochemical profile of 21 patients. Ann Neurol 8:155-160, 1980
T h e syndrome of nonketotic hyperglycemic coma-a
state of severe hyperglycemia, hyperosrnolality, and
dehydration with minimal or no ketoacidosisresults in a mortality of 30 to 60% [2,23]. T h e survival rate is better if the condition is recognized before
impairment of consciousness occurs [15, 24, 251. I n
1973 w e reported 5 cases of nonketotic hyperglycernia ( N K H ) and epilepsia partialis continua (EPC)
[24] and emphasized that EPC may be an initial
symptom of NKH occurring while t h e patient is still
alert.
We have n o w cared for a total of 21 patients with
NKH w h o presented with EPC and have found EPC
to be frequently associated with NKH, once it is
looked for.
Presentation of Patients
Twenty-one patients (11 men and 10 women) with N K H
and EPC were studied (Table 1). One patient (No. 2 1)had
2 episodes of EPC occurring nine months apart; consequently, the following data deal with 22 episodes in 21
patients. EPC consisted of repetitive, nonspreading clonic
muscular twitchings affecting a limited part of the body in a
continuous fashion and lasting from several hours to several days.
The average age of the patients was 61 years, ranging
from 33 to 76 years. The average duration of EPC prior to
admission to the hospital was 4.8 days (range, 0 to 2 1 days)
and the average total duration was 8 days (9 hours to 25
days). In 11 patients EPC was localized to the right side,
From the Department of Neurology, New York Medical
College-Metropolitan Hospital Center, New York, NY.
Received June 11, 1979, and in revised form Dec 10. Accepted for
publication Dec 16, 1979.
and in 10 to the left. Three of the 2 1 patients had one grand
ma1 seizure in addition to the EPC.
Fourteen patients were alert, 2 lethargic, 1 confused, 4
stuporous, and 1 comatose at the time of hospitalization.
Twelve patients were known diabetics. Of these, 4 were
receiving insulin; 5 were being managed by oral antidiabetic medication and 3 by diet alone. In 9 patients, EPC
was the first symptom leading to the diagnosis of diabetes
mellitus.
Thirteen patients had considerable evidence of a structural lesion on the appropriate side of the brain. In 1 (Patient 8) an area of infarction was found on autopsy. In 2
patients (Nos. 19 and 21), there were focal areas of decreased density on CT scan. Three patients (Nos. 7, 14, and
18) had arteriographic evidence of vascular occlusions of
the middle cerebral artery or its branches, and all 3 had
shown clinical evidence of a cerebrovascular accident preceding the EPC. Three other patients (Nos. 2, 15, and 1 7 )
had focal abnormal increased uptake or radioisotope with
radionuclide brain scans using technetium, while 1 (Patient
1) had focal decreased perfusion in a dynamic radionuclide
scan. Of these last 4 patients, 2 continued to have residual
signs from the cerebrovascular accident. Of the remaining
3 patients (Nos. 4 , 5 , and 9), 2 had residual hemiparesis
long after cessation of the seizures, and 1 had had a previous stroke with focal seizures in the same extremity.
Three patients had underlying conditions that might
have caused embolization in the brain: 1 (Patient 16) had a
prosthetic aortic valve and atrial fibrillation and was receiving Coumadin, while 2 (Patients 10 and 11) were heroin addicts.
Address reprint requests to Brij M. Singh, MD, Department of
Neurology, Metropolitan Hospital-Room 13 16, 1901 First Ave,
New York, TXY 10029.
0364-5134/80/080155-06$01.25 @ 1978 by Robert J. Strobos
155
Table 1. Data in 21 Cases of Epilepsia Partialis Continua Associated with Nonketotic Hyperglycemia
EPC Duration (days
before admissiodtotal)
Neurological Deficit
on Admission
1. 43, F
3/14
Alert; aphasia and R facial
weakness
2. 6 1 , M
315
3. 72, F
215
Alert; L hemiparesis and L
hemianopia
Alert; L hemiparesis
4. 69, M
5 . 59, F
717
7/15
Stupor; R hemiparesis
Alert; none
6. 65, M
7. 69, F
111
010.4
Coma; LUE weakness
Alert; L hemiparesis
8. 74, M
7/15
Alert; L hemiparesis
9. 73, F
10. 48, M
11. 3 3 , M
117
717
319
Alert; RLE weakness
Stupor; RUE weakness
Alert; RUE weakness
12. 70, M
7/10
Alert; R hemiparesis
13. 61, F
14. 72, M
111
213
Lethargic; R hemiparesis
Stupor; R hemiplegia
15. 5 3 , M
212
Confused; L hemiparesis
16. 6 1 , F
17. 62, F
4 5
112
Alert; LUE weakness
Lethargic; R hemiparesis
and aphasia
18. 7 6 , F
014
Stupor; R hemiparesis
19. 58, M
216
Alert; L facial and LUE
weakness
20. 58, F
21a. 56, M
2 1125
10117
Alert; LUE weakness
Alert; none
21b. 5 7 , M
14/15
Alert; none
Patient No.,
Age (vr). and Sex
Additional Data
Decreased perfusion in left anterior
hemisphere on flow radionuclide
brain scan
Focal abnormal uptake on static
radionuclide brain scan
Died of acute myocardial infarction, no
autopsy
...
Cerebral angiogram: generalized arteriosclerosis
...
EEG during seizure: intermittent R
frontal sharp- and slow-waves; angiogram: missing branches of R middle
cerebral artery
EEG during seizure: PLEDs; died of
paralytic ileus and GI bleeding; autopsy: renal carcinoma, recent R occipital infarction, and atrophy of R
frontal gyri
...
EEG during seizure: L temporal seizure
discharges
EEG during seizure: L temporal seizure
discharges
...
Angiogram: missing branches of L middle cerebral artery in parietal area;
died of septicemia, no autopsy
Focal abnormal uptake o n static
radionuclide brain scan
...
EEG during seizure: PLEDs; focal abnormal uptake in static radionuclide
brain scan
Angiogram: occlusion of R middle cerebral artery; died of cardiopulmonary
arrest, no autopsy
C T scan: focal area of decreased density
L frontal, and gyral atrophy of R
hemisphere
C T scan: normal
CT scan: focal area of decreased density
in R posterior temporal region
CT scan: normal
LUE = left upper extremity; PLED = periodic lateralized epileptiform discharge; GI = gastrointestinal;RLE = right lower extremity; RUE
= right upper extremity.
All the patients suffered from diabetes mellitus, which
frequently causes complications of microangiopathies and
small ischemic areas. Also, 6 of the patients had a history
of hypertension and 2 of myocardial infarction.
Death occurred in 4 patients (Nos. 3 , 8, 14, and 18)
within 4 to 25 days from hospitalization. All had serious
associated illnesses. O n e patient (No. 3) died of acute myocardial infarction and another (Patient 18) of cardiopulmo-
156 Annals of Neurology Vol 8 No 2
August 1980
nary arrest. O n e patient (No. 14) developed pneumonitis
and urinary tract infection and died of septicemia three
weeks after hospitalization. O n e patient (No. 8) developed
paraplegia, paralytic ileus, and gastrointestinal bleeding and
died of this 25 days after hospitalization. An autopsy revealed renal carcinoma and thinned-out, brownish gray
right occipital cortex due to infarction.
T h e patients' seizures, in general, were resistant to an-
ticonvulsant medication but ceased with correction of the
metabolic disturbances o r with the development of increasing hyperosmolality and stupor.
Electroencephalograms were obtained during clinical
seizures in 9 patients. In 4 of these the record was so distorted by movement artifact that no reliable interpretation
was possible. Two patients had periodic lateralized epileptiform dischwges that correlated with the clonic contractions. Two others had more complicated focal discharges in
the temporal region, which alternated between rhythmic 4
to 5 per second activity and 2 to 3 per second sharp- and
slow-wave frequencies. These discharges at times remained
focal, but sometimes they spread bilaterally with continuing focal preponderance. The clinical seizures were not always fully correlated with the electrical discharges: usually
the 2 to 3 per second sharp- and slow-wave frequencies
were associated with clinical seizures, but at times the discharge was no longer visible while the seizure continued.
Some of these seizures evidently must be associated with
subcortical discharges alone. In 1 patient there was only
intermittent focal sharp- and slow-wave activity that had no
definite time relationship to the EPC.
Eight patients had electroencephalograms only after
cessation of seizure activity. Of these, 2 showed a spike
focus in the appropriate location, 3 had evidence of a
slow-wave focus, while 3 were normal. No electroencephalograms were obtained in the remaining 5 patients.
Lumbar puncture was performed in 14 patients, and increased cerebrospinal fluid pressure (200 to 370 mm H,O
in the lateral decubitus position) was found in 4. Cerebrospinal fluid glucose levels ranged from 132 to 500 mg/dl,
and this represented 47 to 73% of simultaneous blood glucose levels. Six patients had elevated total protein contents
(50 to 105 mgldl) in their cerebrospinal fluid.
Biochemical Data on Admission
The mean blood glucose level was 690 mgldl (range, 32 1 to
1,509); serum sodium concentration, 131.6 mEq/liter (118
to 153); serum potassium, 4.95 mEq/liter (3.8 to 6.9);
serum chloride, 89.9 mEq/liter (75 to 115); serum carbon
dioxide, 21.7 mEq/liter (11.5 to 33); serum blood urea nitrogen 31.4 mgidl ( 9 to 105); and calculated serum osrnalality, 311 mOSm/liter (278 to 372) (Table 2).
Fifteen patients had serum sodium levels below normal
(118 to 134 mEq/liter), 6 had normal levels, and only 1
(Patient 14) had increased serum sodium and chloride
levels. This last patient suffered from pneumonitis, acute
urinary tract infection, and renal failure, with a markedly
elevated blood urea nitrogen, and he died after three weeks
of hospitalization. Seventeen patients had lowered serum
Table 2. Biochemicul Data in 21 Cases of Epilepsia Partialis Continua Associated with Nonketotic Hyperglycemia
Patient
NO.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
2la
21b
Mean
SD
Normal
value
Blood
Glucose
(mddl)
Serum
Sodium
(mEq/L)
Serum
Potassium
(mEq/L)
Serum
Chloride
(mEq/L)
341
534
550
880
430
450
330
495
700
1,509
825
530
1,320
980
1,320
130
125
133
128
131
138
134
136
118
123
130
120
136
153
138
134
136
142
6.9
75
83
92
96
86
94
92
91
92
75
90
83
88
115
92
94
96
95
32 1
480
5 10
940
481
650
596
690
331.4
80-120
5.6
4.8
3.9
5.3
3.8
4.8
128
4.0
4.2
6.2
4.4
4.8
6.9
6.0
5.7
4.2
4.2
5.3
5.8
4.1
4.2
3.9
131.6
7.63
135-145
4.95
0.94
3.5-5
122
128
132
"Serum osmolality (mOSmlL) = 2 x [sodium (mEq/L)
Serum
co,
(mEq/L)
24.5
26
(mddl)
18.5
18
17
22
15.5
24
11.5
20
20
33
20.5
24
21
16
29
19
18
82
25
19
26
26
89.9
8.18
95-105
BUN
9
29
35
39
84
95
a7
Serum
21.7
4.77
24-32
Serum
Qsmolality "
(mOSm/L)
19
18
18
36
32
9
19
46
105
41
23
39
35
31
24
35
31
293
291
306
313
296
309
296
307
283
342
315
278
359
372
361
294
307
323
308
291
309
297
31.4
18.96
311
23.59
10-20
28U
?
10
+ potassium (mEq/L)] + blood glucose (mgldl) + 18.
Singh and Strobos: Epilepsia Partialis Continua and Nonketotic Hyperglycemia
157
chloride levels (75 to 94 mBq/literj, and 1 patient (No. 14),
as mentioned, showed an increased level. Thirteen patients
had lowered serum carbon dioxide levels (11.5 to 23
mEq/liter), and only 1 (Patient 11) had a minimal elevation
(33 mEq/liter). Fifteen patients had raised blood urea nitrogen (23 to 105 mEq/liter); 14 had a mild elevation (23 to
46 mEq/liter) and only 1 patient (No. 14) had a marked
increase. Twenty patients had hyperosmolality (291 to 372
mOSm/liter), but most of them only to a minimal or mild
degree; there were only 4 patients (Nos. 10, 13, 14, and
15) with serum osmolality above 330, which by Plum and
Posner's standards [17] is the threshold for occurrence of
major neurological changes.
A more detailed analysis was underaken to scrutinize the
relationship of the biochemical abnormalities to level of
consciousness, duration of seizure manifestations, and fatal
outcome.
Level of Consciousness
For statistical analysis, patients who were alert (Nos. 1, 2,
3, 5, 7, 8, 9, 11, 12, 16, 19, 20, 21a, and 21bj or mildly
lethargic (Nos. 13 and 17) were pooled in a single group
(16 episodes in 15 patients) and compared with confused
(No. 15), stuporous (No. 4 , 10, 14, and 18j, and comatose
(No. 6) patients in a second group ( 6 patients) (Table 3).
The blood glucose levels in patients with a depressed
level of consciousness ranged from 450 to 1,509 mgldl, and
there was considerable overlap with the patients who were
conscious, who showed a range from 321 to 1,120 mgidl.
Nevertheless, the blood glucose levels were significantly
higher in patients with a depressed sensorium (942 ? 387
mgldlj as compared to conscious patients (595 k 249
mgldl) (p < 0.05). Also, patients with depressed sensorium
had significantly higher levels of serum osmolality (337 t
23.7 mOSm/liter) as compared to values of 302 4 17.6
mOSm/liter in conscious patients (p < 0.01). The serum
sodium levels were not significantly different in the two
groups. Patients with depressed sensorium had significantly
1.92 comlower levels of serum carbon dioxide (18.2
pared to 23 4.85)
The stuporous patients thus had significantly higher
values of blood glucose and serum osmolality and lower
serum carbon dioxide levels as compared to conscious patients: a worse biochemical profile.
*
*
Duration of EPC
For statistical analysis, patients with a total EPC duration of
more than 5 days were included in one group (12 episodes
in 11 patients) and the rest in a second group (10 episodes).
There was no significant difference in the blood glucose
levels and serum osmolality of the two groups. However,
the serum sodium, chloride, and blood urea nitrogen levels
were significantly lower in patients with a longer duration
of EPC (Table 4). The most significant difference was in the
serum sodium level, it being 127 t 5.1 mEq/liter in patients with EPC of 5 days or longer and 137 T 6.8 mEqf
liter in those with EPC for less than 5 days (p < 0.01).
Thus, patients with a prolonged duration of EPC had more
severe hyponatremia.
Table 1 shows the duration of EPC (before admission
and total duration) in the 6 stuporous patients (Nos. 4, 6,
158 Annals of Neurology Vol 8 N o 2
August 1980
Table 3. Comparison of Data
in Conscious and Stuporous Patients
Determination
Blood glucose (mg/dl)
Serum sodium (mEq/LJ
Serum C 0 2 (mEq/L)
Serum BUN (mg/dl)
Serum osmolality
(mOSm/L)
Conscious
Pauents
(16 episodes)
Stuporous
Patients
16 eDisodes)
Significance
595 ? 249
13Ok 5.5
23 ? 4.85
26 ? 9.8
302 2 17.6
942 2 387
137 ? 9.7
18.2 2 1.92
45 5 27 2
337 ? 23.7
P
P
p
p
P
< 0.05
< O.lOa
< 0.01
< 0.10.1
< 0.01
"Not statistically significant.
Table 4. Comparison of Data in Relation
t o Totul Duration of Seizures
Determination
Blood glucose (mg/dl)
Serum sodium (mEq/L)
Serum chloride (mEq/L)
Serum BUN (mg/dl)
Serum osmolality
1rnOSmiL)
EPC > 5 Days EPC S 5 Days
112 eoisodes) (10eoisodes) Sienificance
698 +- 307
127 ? 5.1
86 f 6.7
25 k 10.0
303 ? 16
680 2 363
137 2 6.8
94 ? 7.8
39 2 23.7
322 2 29
P < 0.10"
p
P
p
p
< 0.01
< 0.05
< 0.05
< O.lOa
"Not statistically significant.
10, 14, 15, and 18). Depression of consciousness was associated with cessation of EPC in the majority of the patients,
suggesting that increasing hyperosmolality may have decreased their susceptibility to EPC.
Fatal Outcome
Of the 4 patients who died, 2 (Nos. 3 and 8) were alert and
2 (Nos. 14 and 18) were stuporous o n admission. These
patients were significantly older (74 t 1.6 years) than those
who survived (59 5 9.9 years) (p < 0.05). All were
longstanding diabetics. They had significantly higher initial
levels of serum sodium (141 ? 8 mEq/liter) and serum
chloride (98 ? 10 mEq/liter) than the patients who survived
(serum sodium, 129 5 6.05 mEq/liter; serum chloride, 88
6.41 mEq/liter) (p < 0.05 j. The serum blood urea nitrogen
and osmolality levels were also slightly higher in the patients who died.
These patients, as has been discussed, died of serious associated illnesses, but it was, nevertheless, in the setting of
a worse biochemical profile.
*
Discussion
The syndrome of EPC has been described in association with a variety of focal cerebral lesions [l, 3, 5,
11-13, 18, 22, 271. Recently the subject has been
reviewed in detail by Thomas, Reagan, and Klass
[ 281.
In 1973 we [24]presented 5 patients who had EPC
as the initial feature of NKH. We also reviewed 158
cases of NKH reported in the English-language literature: 40 patients (25%) had seizures, 30 of these
having focal motor seizures (19% of the total group).
Ten of these 30 (6% of the total) had repetitive focal
motor seizures as their initial symptom prior to the
onset of coma.
The present data show that in the majority of pa-
tients, EPC occurs in the early stages of N K H , prior
to the onset of coma, in a setting of moderate hyperglycemia, hyponatremia or normonatremia, and mild
hyperosmolality. Even though the pathogenesis of
EPC in N K H remains uncertain, it is clear that most
of these patients have a definite organic cerebral
lesion in the appropriate location. The metabolic
abnormalities most likely influence the epileptic
threshold, enhancing the epileptogenic effect of the
lesions. This is suggested by the clinical data in Patient 21, who presented with EPC involving the left
upper extremity. The CT scan showed a small area of
decreased density in the right posterior temporal region. The patient recovered with correction of the
metabolic derangement. Nine months later he again
presented with EPC of the left upper extremity in a
state of N K H and hyponatremia. The C T scan this
time was normal. It seems, therefore, that the metabolic abnormality triggered epileptic discharges in
the area of the previous infarction.
Maccario [14]reported a similar case: a 73-year-old
man with focal right-sided seizures and N K H recovered with treatment but had persistent right
homonymous hemianopia. Ten months later he again
suffered from an episode of N K H and had recurrence of focal seizures on the right side.
A critical review of 20 patients with N K H and
repetitive focal seizures by Daniel, Chokroverty, and
Barron [6] also suggests that cerebrovascular disease
played an important role in the causation of focal seizures. Focal neurological changes have been observed in the absence of seizure activity as presenting
features in NKH preceding the development of
coma [2, 6, 141.
Chatrian et a1 [ 4 ] reported on 33 patients with
periodic lateralized epileptiform discharges in the
electroencephalogram, of whom 29 experienced
focal epileptic seizures. The great majority of these
patients suffered from cerebral infarction. Only 7
presented with typical EPC, and of these, 6 had cerebral infarcts. Eleven of the 33 patients had a diagnosis
of diabetes mellitus.
In the literature, the role of serum hyperosmolality
has been stressed as a cause of repetitive focal seizures in N K H . Experimental and clinical observations by Vastola, Maccario, and Homan [291 suggest
that serum hyperosmolality and brain dehydration
are a sufficient explanation for the occurrence of seizures, given the condition of a potentially epileptogenic process. Experimentally, focal seizures have
been induced by administration of hypertonic solution [7, 261. The majority of patients in the present
report had only mild serum hyperosmolality even
though they had had EPC for a few days prior to hospitalization. Thus, even though EPC occurred in the
setting of mild hyperosmolality, seizures in these patients ceased as hyperosmolality increased and de-
hydration occurred. There is a direct relationship
between degree of serum hyperosmolality and depression of the sensorium, and in this aspect our data
are in agreement with the observations of others 12,
10, 161.
Hyponatremia was a major abnormality in most of
these 21 patients, especially in those with a prolonged duration of EPC. Low serum sodium levels in
the syndrome of N K H have also been reported by
others [6, 20, 211. Arieff and Carroll 121 reported
serum sodium levels of 127 -+ 5 mEq/liter in 4 patients with hyperglycemia without coma, as compared to 144 2 11 mEq/liter in those with NKH
coma. Five of the 7 patients with repetitive focal seizures and N K H reported by Maccario et a1 [141 had
serum sodium levels ranging between 125 and 130
mEq/liter.
In 2 of the 9 cases of EPC described by Juul-Jensen
and Denny-Brown [ 121, hyponatremia was present.
In 1 of these, the lowest serum sodium values (range,
121 to 137 mEq/liter) were found when the patient
had seizures. In the opinion of these authors, “the
disturbances in the electrolytes may have been of importance for the continuous course of twitches” because the pathological findings indicated widespread
edema surrounding the lesion.
I n the study by Chatrian et a1 [ 4 ] ,7 of the 33 patients had evidence of hyponatremia, though other
metabolic disturbances were also reported.
In experiments intended to differentiate between
the roles of sodium and of hyperosmolality in producing focal neurological deficit in animals that had
suffered infarction of the brain as a result of ligation
of the middle cerebral artery, Espinas and Poser [9]
concluded that the resulting hemiparesis is related to
hyponatremia rather than to changes in osmolality.
The authors thought it conceivable that in patients
with N K H coma, the hyponatremia which may be
present in the initial phase might no longer be clinically detectable by the time the patients are hospitalized. The increasing degree of dehydration may
result in fallaciously elevated serum sodium levels.
Marked hyperglycemia in the presence of hyponatremia with normal serum osmolality was not accompanied by neurological dysfunction in nondiabetic
patients who developed hyperglycemia postoperatively due to intravenous glucose infusion [30]. It appears that hyperglycemia and hyponatremia precipitate EPC in patients with N K H only when where
is an associated structural lesion in the brain.
Seizures are rare in diabetic ketoacidosis. yAminobutyric acid (GABA) is a presumed inhibiting
substance in the central nervous system. Intracellular
alkalosis decreases the content of GABA in the central nervous system [191, possibly due to lack of
synthesis-since glutamic acid decarboxylase needs
an acidotic pH-and because of increased transami-
Singh and Strobos: Epilepsia Partialis Continua and Nonketotic Hyperglycemia 159
nation to succinic semialdehyde, which is enhanced
by an alkaline pH. Brain glucose utilization is reduced in both diabetic ketoacidosis and N K H . In
ketoacidosis, most of the brain energy requirements
are derived from ketone bodies; since ketones are
not available in NKH, however, an increased rate of
GABA utilization via the GABA shunt may be one
of the sources of energy requirements, thereby
further lowering the GABA level and reducing the
threshold for seizure activity.
A patient with diabetic ketoacidosis was reported
[8] in whom right-sided focal seizures developed
during therapy. At that time the serum sodium level
had fallen to 120 mEq/liter although the blood glucose ievel was only 209 mgldl ( value on admission,
425 mg/dl). At the same time the blood bicarbonate
level had risen to 17 mEq/liter from 3 mEq/liter on
admission. The focus of interest in this case is that
focal seizures occhrred during a phase of hyponatremia associated with lack of ketoacidosis.
It seems, therefore, that an acute infarct or an old
lesion-a scar formation-is triggered to produce
focal epileptic activity by the superimposed metabolic disturbances associated with N K H .
It is important to recognize that EPC occurs in the
early stages of N K H , when patients are alert and in a
hyponatremic or normonatremic and only mildly
hyperosmolar state. At this point, recovery without
serious sequelae is possible. This stage should be
differentiated from nonketotic hyperglycemic coma,
when EPC ceases and increasing hyperosmolality and
dehydration may result in an increased mortality.
Patients who present with EPC should have immediate determination of blood glucose levels. The
findings may lead not only to the diagnosis of previously unsuspected diabetes mellitus, but also to the
appropriate treatment for their seizure disorder and
prevention of further neurological deterioration.
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profil, associates, patients, clinical, partiality, epilepsies, hyperglycemia, nonketotic, continue, biochemical
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