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Neurological Conditions

Neurological Conditions like Wernicke's Encephalopathy and Central Pontine Myelinolysis are easily treated, but most likely to cause a fatal result for the mother and unborn child if left untreated. Increasing numbers of cases are being reported each year. Symptoms differ in non-alcoholic patients like mothers with HG.

See our new published Case Study on HG and WE/CPM/EPM for recommendations on identification, prevention and treatment.

WE is typically identified by the symptom triad of ataxia, confusion and oculomotor abnormalities. However, 10-47% of patients lack these signs, especially with ... non-alcoholic [HG] patients... Persistent or prolonged vomiting, confusion, and unintentional weight loss are red flags indicating a high risk of WE. Additional WE signs ... include weakness, dysarthria, confabulation, akinetic mutism, aphasia, cardiac failure, seizures, abdominal pain and nausea. Mental status changes are nearly universal and exhibited as dizziness, drowsiness, apathy, and cognitive impairment. Gait abnormalities range from weakness to inability to stand...

MacGibbon K, Fejzo M, Mullin P. Mortality Secondary to Hyperemesis Gravidarum: A Case Report. Women’s Health & Gynecology. 2015;1(2):011.

Wernicke's Encephalopathy

Signs: Vision and mental status changes, gait abnormalities, weakness, dysarthria, confabulation, and coma.

Unfortunately, Wernicke’s Encephalopathy (WE) is too common in hyperemesis gravidarum due to malnutrition, yet is very often goes unrecognized until significant and potentially permanent morbidity occurs. It can be fatal in up to 20% of cases, and may even cause spontaneous abortion (miscarriage).

It is caused by vitamin deficiencies, most notably thiamin (B1) deficiency, and precipitated by administration of glucose-containing fluids before deficiences are corrected. Lab values of hormones, other electrolytes, and nutrients can vary as is shown in the research, thus lab results should not be used solely to determine a diagnosis. Further, it should not be assumed that women on TPN will not have Wernicke’s Encephalopathy. TPN often does not include a complete vitamin profile and these women are still at risk. Even MVI infusion only has 6 mg of thiamine and it is recommended much higher doses be given to HG mothers. It is highly recommended that women receive 100 mg of thiamine in their IV fluids or preferably, B complex daily.

Women may present with the classic triad of symptoms, visual disturbances, confusion and muscular weakness. Early intervention with thiamine replacement is typically all that is needed to prevent this complication. Wernicke’s Encephalopathy (WE) can develop after just a few weeks of vomiting. Women vomiting more than one week should be routinely given thiamine replacement, along with a parenteral multivitamin, prior to IV fluids with glucose.

Offsite Info on Wernicke's Encephalopathy:

Central & Extra Pontine Myelinolysis (Osmotic Demyelination Syndrome, ODS)

Classic Signs: Confusion, loss of consciousness, horizontal gaze paralysis, and spastic quadriplegia.

Women with HG may also exhibit signs of extra and ODS, other neurological disorders caused by electrolyte shifts, most commonly when low sodium or potassium levels are corrected too quickly. Signs include confusion, horizontal gaze paralysis, and spastic quadriplegia. Delirium is also very common. ODS also has a high rate of morbidity related to demyelination of the pons.

It is not uncommon for pontine myelinolysis and Wernicke’s Encephalopathy (WE) to occur simultaneously with other disorders related to malnutrition and electrolyte disturbances. Women with HG should be monitored closely and given nutritional support and methodical electrolyte replacement to prevent maternal and/or fetal morbidity and mortality.

Offsite Info on Central Pontine Myelinolysis:

Offsite Research:

Hyperemesis gravidarum complicated by Wernicke's encephalopathy.
Spruill SC, Kuller JA.
Department of Obstetrics and Gynecology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Obstetrics & Gynecology 2002 May;99(5 Pt 2):875-7

Wernicke's encephalopathy is usually associated with alcohol abuse, but can also occur with hyperemesis gravidarum. The effect of delay in thiamine replacement on fetal outcomes is unknown. We present a case of this complication. CASE: A primipara with hyperemesis was admitted for mental status changes in her 14th week of pregnancy. Physical examination revealed a lethargic patient with ophthalmoplegia, ataxia, and hyporeflexia. Parenteral thiamine therapy was started. The patient improved rapidly although the ataxia persisted. A spontaneous abortion occurred 2 weeks later. CONCLUSION: Wernicke's encephalopathy can complicate hyperemesis gravidarum. Early thiamine replacement may decrease the chances of spontaneous abortion.
 

Threatening thiamine deficiency in severe hyperemesis gravidarum. (article in German)
Fischer J, Muller A, Pohl C, Jens H.
Universitatsfrauenklinik, Abteilung Innere Medizin I, Tubingen, BRD.
Schweizerische Medizinische Wochenschrift 1993 Mar 13;123(10):428-31

We report the case of a patient with severe hyperemesis gravidarum. During parenteral nutrition the patient developed threatening thiamine deficiency. Wernicke's encephalopathy and tachycardia were predominant in the clinical course. Severe lactic acidosis and prolonged prothrombin time were the leading laboratory features. Thiamine deficiency as a cause of severe metabolic acidosis or coma can be easily ruled out or validated by intravenous thiamine administration.
 

Memory loss and ataxia after hyperemesis gravidarum: a case of Wernicke-Korsakoff syndrome.
Accetta SG, Abeche AM, Buchabqui JA, Hammes L, Pratti R, Afler T, Capp E.
European Journal of Obstetrics, Gynecology, and Reproductive Biology 2002 Apr 10;102(1):100-1

Hyperemesis gravidarum can induce Wernicke-Korsakoff syndrome (WKS), a thiamin deficiency disorder characterized by ocular abnormalities, ataxia and disturbance of consciousness. This should be considered in the differential diagnosis of pregnant patients with persisting vomiting and neurological alterations.
 

Wernicke's encephalopathy in hyperemesis gravidarum.
Kim YH, Lee SJ, Rah SH, Lee JH.
Department of Ophthalmology, Wonju Christian Hospital, Yonsei University Wonju College of Medicine, Wonju-city, Kangwon-do, Korea.
Canadian Journal of Ophthalmology 2002 Feb;37(1):37-8

Wernicke's encephalopathy due to hyperemesis gravidarum: an under-recognised condition.
Togay-Isikay C, Yigit A, Mutluer N.
The Australian & New Zealand Journal of Obstetrics & Gynaecology 2001 Nov;41(4):453-6

We present a case of a 25-year-old woman with drowsiness, nystagmus, severe ataxia and areflexia, which developed six weeks after admission to an obstetric clinic for hyperemesis gravidarum. She had been treated with intravenous dextrose and electrolyte solutions and antiemetics. Magnetic resonance imaging (MRI) performed on the fifth day of her neurologic symptoms showed increased intensity in both thalami, periaqueductal grey matter, the floor of the fourth ventricle and superior cerebellar vermis in T2 weighted and FLAIR images. Clinical signs and MRI findings were consistent with the diagnosis of Wernicke's encephalopathy. On the third day of thiamine replacement, neurologic signs improved dramatically In addition to our case, we review 29 previously reported cases of Wernicke's encephalopathy associated with hyperemesis gravidarum, and emphasize the importance of thiamine supplementation to women with prolonged vomiting in pregnancy especially if they are given intravenous or parenteral nutrition.
 

Wernicke's encephalopathy in patients with hyperemesis gravidarum.
Tan JH, Ho KH.
Department of Medicine, National University Hospital, Singapore. (e-mail: junetan99@yahoo.com)
Singapore Medical Journal 2001 Mar;42(3):124-5

Our two patients presented with Wernicke's Encephalopathy (WE) resulting from prolonged hyperemesis gravidarum.This is an unusual cause of WE, a potentially fatal medical emergency due to thiamine deficiency. We discuss the clinical settings, presentation, diagnosis, neurophysiological and radiological findings, treatment and outcome of WE in these two cases and the neuropathologic correlation of this condition. We stress upon the importance of early diagnosis and prompt treatment of WE.
 

Wernicke's encephalopathy induced by hyperemesis gravidarum.
Gardian G, Voros E, Jardanhazy T, Ungurean A, Vecsei L.
Department of Neurology, Albert Szent-Gyorgyi Medical University, Szeged, Hungary.
Acta Neurologica Scandinavica 1999 Mar;99(3):196-8

A report is presented on a patient with Wernicke's encephalopathy secondary to hyperemesis gravidarum. The 25-year-old female presented 11 weeks into pregnancy with prolonged vomiting. Neurological examination 8 weeks later demonstrated obtunded sensations, nystagmus and ataxia of gait. MR imaging revealed bilateral lesions in the mediodorsal nuclei of thalami, in the hypothalamus and in the periaqueductal gray matter (1). The neurological signs and the MRI findings pointed to a diagnosis of Wernicke's encephalopathy. The patient was treated with intramuscular vitamin B1 followed by oral thiamine until the end of pregnancy. The subsequent course of the pregnancy was uncomplicated, and resulted in the delivery of a healthy 2970 g male infant. A review of the literature published during the last 30 years revealed an additional 20 cases of Wernicke's encephalopathy induced by hyperemesis gravidarum. Only half of these pregnancies resulted in the birth of a normal infant.
 

[Central pontine myelinolysis induced by hyperemesis gravidarum] [Article in Spanish]
Tonelli J, Zurru MC, Castillo J, Casado P, Di Prizito C, Gutfraind E.
Departamento de Clinica Medica y de Neurologia, Hospital Santojanni, Argentina.
Medicina (B Aires) 1999;59(2):176-8

An 18-year-old woman in her first pregnancy with hyperemesis gravidarum, presented dehydration, without hyponatremia. She was confused with profound disorientation, apathy, and drowsiness. She presented upbeating nistagmus on upward gaze and gate ataxia recognised as Wernicke's encephalopathy. Laboratory tests demonstrated hypokalemia, hypernatremia and aminotransferase elevation. The serum osmolality was 319 mOsm/kg and the water deficiency 2.73 l. The patient developed weakness in the four limbs, with hypotonicity, absence of tendon reflexes and showed bilateral Babinski signs. A T2 weighted sagittal cranial-magnetic resonance imaging revealed a high signal within mid-pons suggesting central pontine myelinolysis. In this case we highlight the absence of hyponatremia. Furthermore, the central pontine myelinolysis was probably secondary to hypokalemia, hypernatremia and hyperosmolality.
 

Pregnant, vomiting, and coma.
Hillbom M, Pyhtinen J, Pylvanen V, Sotaniemi K.
Department of Neurology, University Hospital of Oulu, Finland. (e-mail: matti.hillbom@oulu.fi)
Lancet 1999 May 8;353(9164):1584

Pregnant, vomiting, and going blind.
Tesfaye S, Achari V, Yang YC, Harding S, Bowden A, Vora JP.
Department of Medicine, Royal Liverpool University Hospital, UK.
Lancet 1998 Nov 14;352(9140):1594

Two pregnant women with vomiting and fits.
Rees JH, Ginsberg L, Schapira AH.
Department of Neurology, Royal Free Hospital, London, United Kingdom.
American Journal of Obstetrics & Gynecology 1997 Dec;177(6):1539-40

Two women with hyperemesis gravidarum were first seen with a short history of confusion diplopia, unsteadiness, and fits caused by Wernicke's encephalopathy. The neurologic presentation had been precipitated by a carbohydrate load inadvertently administered without vitamin supplementation. We stress the importance of prescribing thiamine supplements to all women with prolonged vomiting during pregnancy.
 

[Gayet-Wernicke encephalopathy and centropontine myelionolysis induced by hyperemesis gravidarum] [Article in French]
Olindo S, Smadja D, Cabre P, Mehdaoui H, Heinzlef O.
Service de Neurologie, CHU Fort-de-France, Martinique.
Reviews of Neurology (Paris) 1997 Jul;153(6-7):427-9

A 24-year-old woman developed hyperemesis gravidarum, complicated by Wernicke's encephalopathy and central pontine myelinolysis. The first-was due to a deficiency of thiamine, and was hastened by intravenous dextrose without thiamine supplements. However, no changes in serum sodium or phosphorus values were observed. In this case, the pathophysiology of central pontine myelinolysis remained obscure.
 

Gestational thyrotoxicosis manifesting as wernicke encephalopathy: a case report.
Otsuka F, Tada K, Ogura T, Hayakawa N, Mimura Y, Yamauchi T, Inoue N, Makino H, Kudo T.
Department of Medicine III, Okayama University Medical School, Japan.
Endocrinology Journal 1997 Jun;44(3):447-52

The thyroid gland is physiologically stimulated in normal early pregnancy. This stimulated thyroid function is occasionally termed "gestational transient thyrotoxicosis". The cause of this thyrotoxicosis has been clarified to closely it associate with human chorionic gonadotropin (hCG). We encountered a pregnant patient with hyperemesis and thyrotoxicosis, who manifested symptoms of Wernicke encephalopathy. Although her serum hCG concentration transiently increased in accordance with the thyrotoxicosis, it was within normal limits for the gestational week. Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy. This case suggests that pregnant patients with hyperemesis should undergo careful endocrinological and neurological evaluations.
 

Micturitional disturbance in Wernicke's encephalopathy.
Sakakibara R, Hattori T, Yasuda K, Yamanishi T, Tojo M, Mori M.
Department of Neurology, Chiba University School of Medicine, Japan.
Neurourology and Urodynamics 1997;16(2):111-5

A 24-year-old pregnant woman started to have hyperemesis gravidarum 6 weeks before admission. Four weeks later she had vertigo, diplopia, staggering gait, mild dyspnea, dysphagia, and incontinence of urine. On admission she presented with ophthalmoplegia, ptosis, ataxia, decreased tendon reflex, and memory disturbance. Brain magnetic resonance imaging revealed abnormal intensities in medial thalamic-hypothalamic regions and the periaqueductal area, and she was diagnosed with Wernicke's encephalopathy. Urodynamic studies revealed decreased bladder volume and detrusor hyperreflexia. Six weeks after the administration of 100 mg/day of thiamine, urge incontinence gradually recovered, together with neurological signs. Lesions of the medial thalamic-hypothalamic area and the periaqueductal gray matter seemed to be mainly responsible for micturitional disturbance in our patient with Wernicke's encephalopathy.
 

Acute Wernicke's encephalopathy associated with hyperemesis gravidarum: magnetic resonance imaging findings.
Omer SM, al Kawi MZ, al Watban J, Bohlega S, McLean DR, Miller G.
Department of Medicine, King Khalid National Guard Hospital, Jeddah, Saudi Arabia.
Journal of Neuroimaging 1995 Oct;5(4):251-3

A 25-year-old woman with hyperemesis gravidarum developed acute Wernicke's encephalopathy during prolonged intravenous fluid therapy without vitamin supplements. Delay in diagnosis led to a persistent severe neurological deficit, including coma. Gadolinium-diethylenetriaminepentaacetic acid-enhanced magnetic resonance imaging revealed symmetrical lesions around the aqueduct and fourth ventricle, which resolved after treatment with thiamine. She did not regain consciousness. This report demonstrates the diagnostic value of enhanced magnetic resonance imaging in acute Wernicke's encephalopathy.
 

[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum] [Article in Japanese]
Iwamoto Y, Okuda B, Miyata Y, Tachibana H, Sugita M.
Fifth Department of Internal Medicine, Hyogo College of Medicine.
Rinsho Shinkeigaku. Clinical Neurology. 1994 Jun;34(6):599-601

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
 

Wernicke's encephalopathy and central pontine myelinolysis induced by hyperemesis gravidarum.
Peeters A, Van de Wyngaert F, Van Lierde M, Sindic CJ, Laterre EC.
Service de Neurologie, Cliniques Universitaires St. Luc, Universite Catholique de Louvain, Brussels, Belgium.
Acta neurologica Belgica 1993;93(5):276-82

A 21-year-old woman developed hyperemesis gravidarum, complicated by Wernicke's encephalopathy and central pontine myelinolysis. For the latter, time course of the lesions on magnetic resonance imaging suggests a pathogenetic role for hypophosphatemia rather than for hyponatremia.
 

Wernicke's encephalopathy: a predictable complication of hyperemesis gravidarum.
Lavin PJ, Smith D, Kori SH, Ellenberger C Jr.
Obstetrics & Gynecology 1983 Sep;62(3 Suppl):13s-15s

Wernicke's encephalopathy occurred during prolonged intravenous feeding in two patients with hyperemesis gravidarum. Delay in diagnosis caused a protracted illness and persisting neurologic deficits in both patients. Because of its association with chronic alcoholism, the possibility of Wernicke's encephalopathy may not be considered early enough, if at all, in other situations; it is too frequently not discovered until postmortem examination. The disease may complicate other neurologic disorders due to nutritional deficiency, but can be prevented by the timely administration of parenteral thiamine.
 

Wernicke's encephalopathy in early pregnancy complicated by disseminated intravascular coagulation.
Watanabe K, Tanaka K, Masuda J.
Virchows Archiv. A, Pathological Anatomy and Histopathology 1983;400(2):213-8

A 29 year-old Japanese woman with hyperemesis gravidarum became comatose and died. The autopsy revealed a typical case of Wernicke's encephalopathy complicated by disseminated intravascular coagulation (DIC). Repeated vomiting and parenteral nutrition without vitamins led to Wernicke's encephalopathy and a spontaneous abortion 24 h before death triggered the induction of DIC.
 

Updated on: Feb. 10, 2016

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