William R. Morris
Presenting Diagnosis: Likely flavivirus encephalopathy
History of present illness: Upon admission, ‘Stella’ is a 26-year-old female transferred from another hospital with a diagnosis of encephalopathy. The patient was originally noted to complain of right lower extremity weakness in mid-February. Following that, the patient experienced an episode of subjective slurred speech and presented to the emergency room at which time a CT scan and labs were done which were normal, and the patient was discharged with a diagnosis of anxiety and given Ativan p.r.n. The following day, the patient had an episode of presyncope. On February 14 while having dinner, she again complained of right lower extremity numbness and weakness and was noted to have decreased talkativeness. At that time, her family member who is a physician examined her and found no fevers or nuchal stiffness. On February 17, the patient experienced an episode of vomiting 1x followed by seizure-like activity witnessed by her family. Per EMS, the patient experienced seizures for approximately 30 minutes described as flailing of the limbs, tonic-clonic type. This, however, cannot be verified from the previous notes we have obtained from the transfer. The patient was given Ativan without relief, given Dilantin load and eventually transferred into the hospital. The family reported that the patient complained of auditory hallucinations while in the hospital.
Per family description, on February 22, when she was discharged from the hospital and arrived home, she experienced unintentional movements of her bilateral lower extremities described as kicking which eventually progressed to involve her upper extremities as well. At that time she was noted to be looking around but not responding. On February 23, the patient was again admitted and at that time the records indicate she was having bizarre mental affect and catatonic. She was treated with Remaron and Dilanton. EEG at that time was noted to be negative. On February 24, the patient noted to have involuntary movement of her mouth, face and lips, dyskinetic movements like chorea and dystonia. The evaluation at that time was assessed as pseudoseizure and the patient had an additional EEG which showed no abnormalities. The patient continued to have difficulties with these choreoarthetoid –type movements and underwent secondary neurological consultation. She had a lumbar puncture don on March 1 which demonstrated small pleocytosis with a white count of 13 and red blood cells of 1 with 100% lymphocytes. The protein and glucose were within normal limits. The patient had an extensive neurological workup done which revealed seemingly no obvious cause of her encephalopathy. The pateinet had yet a third EEG done at that time which revealed diffuse slowing and triphasic waves. A 14-3-3 protein * was sent off and the diagnosis of prion disease was entertained. The patient continued during her hospitalization to remain alert but impaired awareness and cognition.
On March 3, 2005 the patient was transferred to a neuro ICU for further workup.
Past Medical History: significant for a possible eating disorder as well as depression.
Family History: Patient seemingly has no family history for seizures, neurodegenerative disorders, or other close contacts with contagious or infectious diseases.
Social History: Significant that the patient is the mother of two children, ages 2 and 6, per family member, the patient does not smoke or drink or use drugs. Patient was born in the Philippines in a village where Dengue fever was endemic. The patient visits the Philippines once every two years. Last visit to the Philippines was March 2004. Only recent travel includes a trip to Pachanga CA one month prior to the onset of symptoms. .
Allergies: none known
Hospital Course: In the neuro ICU, the patient was placed on continuous EEG monitoring and she was noted to have diffuse slowing without evidence of epileptic activity. MRI/MRA of the brain was completed on March 26, 2005, which demonstrated normal exam. This normal DWI-weighted imaging of the brain decreased the level of suspicion for prion disease. Later, notification came from the first hospital that the 14-3-3 protein was negative. While in IC, the patient had a brain biopsy performed from the right frontal area. Biopsy shows mild lymphocyte infiltration of the vessels, but no perivascular cuffing and no fibroid necrosis and no other pathological evidence of vasculitis. She was noted to be stable and transferred to the floor. Upon transfer to the floor, the patient’s workup was continued with multiple laboratory tests noted below. At that time, the patient continued to have dyskenetic movements of her oral buccal area as well as her extremities. Also noted to have dystonia in her bilateral lower extremities. The patient continued to track with eyes; however, unresponsi9ve. After discussion, the consideration for the possibility of flavivirus infection was entertained. The outside lumbar puncture had demonstrated a lymphocyte pleocytosis and also the West Nile EgG from the outside hospital was positive. However, IgM was negative. At that time it was determined to pursue the possible diagnosis further for which we sent serum to the Encephalitis project for evaluation of different potential pathogens. Also, day prior to discharge patient had a repeat EEG which demonstrated diffuse slowing without evidence of epileptic activity.
Tongue: red and tender with no coat, no sublingual engorgement
Pulse diagnosis: Thready, wiry – in Shen-Hammer parlance, the pulse was thin, flooding defeicient and urgent. With a systemic infection that targets the nervous system, the surface area of the palpable pulse provides the most salient data regarding the affect on the nervous system. Here the sensation was rather sharp as the wave peaked hard, but without force.
Diagnosis: epidemic heat toxins affecting the wei and ying stage
Herbal Interventions
At this time, there are no proven effective herbal therapies for West Nile Virus and it is doubtful that there will be proof of such effectiveness in the near future. However, herbs have been applied to encephalitis cases in China, and for treatment of viral diseases, including yellow fever.
Subhuti Dharmananda quotes from Modern Study and Application of Chinese Materia Medica 1 which suggests some evidence for the following agents as having anti-arborvirus and clear heat toxin activities: ban lan gen (Fo et Rx Isatis tinctorium) and hu-chang (Polygonum cuspidatum). The Wen Bing model leads directly to medicinals involved in the wei stage or the ying stage depending on the severity and tropism of pathology. At the wei stage the formulas are yin qiao san or sang ju yin. Because of the headache component of mild attacks, my predilection is towards sang ju yin since it can regulate liver qi and resolve headaches while dispelling wind heat. The primary formula for the ying stage is qing ying tang that includes medicnals that clear heat, calm internal wind, and open the orifices. Clear heat herbs include sheng di (raw Rx Rehmannia) mu dan pi (Cx moutan radicis) clear heat from the blood level, huang lian (Rz Coptis chinensis) and huang qin (Rx Scutellaria baicalensus) both drain damp heat; wind calming herbs include uncaria, gastrodia, and silkworm; orifice opening herb therapies include acorus and borneol. 2 1
Conversations with Gu Neiqiang provided some interesting perspective. It begins with wind heat toxins and then progresses to the interior a commonly used prescription for such problems is Qing Wen Bai Du San (Yin) which clears Heat, detoxifies, cools blood and drains Fire.
Shi Gao (gypsum)…60-120g
Zhi Mu (radix anemarrhenae asphodeloidis)…6-12g
Gan Cao (radix glycyrrhizae uralensis)…3-6g
Dan Zhu Ye (herba lophatheri gracilis)…3-6g
Xi Jiao (cornu rhinoceri)…9-12g
Sheng Di Huang (radix rehmanniae glutinosae)…9-15g
Mu Dan Pi (cortex moutan radicis)…6-12g
Chi Shao (radix paeoniae rubrae)…6-12g
Xuan Shen (radix scrophulariae ningpiensis)…6-12g
Huang Lian (rhizoma coptidis)…6-12g
Huang Qin (radix scutellariae)…3-9g
Zhi Zi (fructus gardeniae jasminoidis)…6-12g
Lian Qiao (fructus forsythiae suspensae)…6-12g
Jie Geng (radix platycodi grandiflori)…3-6g
Indications: severe Fire in the Qi and Xue levels. This formula is basically a combination of Bai Hu Tang, Xi Jiao Di Huang Tang, and Huang Lian Jie Du Tang, therefore one can understand it’s usage and power. Powerful high fevers and excessive thirst show Qi level Heat, headache and rashes with general malaise shows Fire toxin, irritability, various bleeding, and rashes show Heat in the Xue level. T- dark red (lips are also dark red), P- rapid and thin or floating and large (if the Fire has penetrated but still partially remains in the superficial levels of the body). If severe the patient may show delirious speech and altering of consciousness.
In a brief conversation with Joseph Yang, PhD, he indicated the following pattern: Toxic wind heat that quickly transfers to the ying and the blood stages causing coma and stupor. The formulas for these patterns include Qing Ying Tang and Xi Jiao Tang.
Xi Jiao (cornu rhinoceri)…9g,
Shui Niu Jiao (water buffalo) is quite often substituted for Rhinoceros horn.
Xuan Shen (radix scrophulariae ningpoensis)…9g
Sheng Di Huang (radix rehmanniae glutinosae)…15g
Mai Men Dong (tuber pohiopogonis japonici)…9g
Jin Yin Hua (flos lonicerae japonicae)…9g
Lian Qiao (fructus forsythiae suspensae)…6g
Huang Lian (rhizoma coptidis)…4.5g
Dan Zhu Ye (herba lophatheri gracilis)…3g
Dan Shen radix salviae miltiorrhizae)…6g
Indications: high fever that is worse at night, Heat disturbs the Heart causing severe irritability, restlessness, and insomnia, dry scarlet red tongue, thin rapid pulse, may be thirsty, delirious, may see faint erythema of the epidermis (if this is present the pathogen is moving into the Xue level). If there is still thirst some of the pathogen remains in the Qi level, if there is no thirst the pathogen has fully entered the Ying level. This formula vents the pathogen through the Qi level. It can be used for epidemic warm febrile diseases such as meningitis, and pneumonia.
From the text Wen Re Jing Wei, the formula Shen Xi Dan
Shui niu jiao
Shi chang pu
Huang qin
Sheng di
Jin yin hua
Ban lan gen
Lian qiao
Xiang zhi
Xuan Shen
Tian hua fen
Zi zao
Wen Hua Bing suggests that the following formulas are commonly selected for this type of case in China:
An Gong Niu Huang Wan will be the first choice
Zi Xue Dan – purple snow powder – used for pediatrics
Zhi Bai Dan phlegm is the predominate pattern
Qing Kai Lin is the primary formula that is used in place of An Gong Niu Huang Wan but the honey ball is too slow, it comes in liquid, IV and tablets.
Ingredients: artificial Niu Huang and other ingredients of An Gong Niu Huang Wan.
Clinical description
Many people who are infected with WNV are asymptomatic. Others may experience mild symptoms, such as low-grade fever, headache and body aches, skin rash, or swollen lymph nodes, within 2 weeks. When the CNS is affected, clinical syndromes ranging from febrile headache to aseptic meningitis to encephalitis may occur, and these are usually indistinguishable from similar syndromes caused by other viruses. WNV meningitis is characterized by fever, headache, stiff neck, and pleocytosis (white blood cells in the cerebrospinal fluid). Arboviral encephalitis is characterized by fever, headache, and altered mental status ranging from confusion to coma with or without additional signs of brain dysfunction (e.g., paresis or paralysis, cranial nerve palsies, sensory deficits, abnormal reflexes, generalized convulsions, and abnormal movements). The symptoms usually clear up in a few days in the mild cases. There is not a specific medical treatment, but palliative care is given for the severe disease, from which about 95% of patients are expected to recover.
Probable case
Confirmed case
The seasonality of arboviral transmission is variable and depends on the geographic location of exposure the specific cycle of viral transmission, and local climatic conditions3.
History of West Nile Virus
West Nile virus, an Old World flavivirus related to St. Louis encephalitis virus was first isolated and identified as a distinct pathogen from the blood of a woman in the West Nile region of Uganda in 1937. Several genetic lineages of the virus have been identified in different geographic locations. Its distribution extends throughout Africa, the Middle East, and southern temperate and tropical Eurasia. During the 1950s, an estimated 40% of the human population in Egypt's Nile Delta was seropositive for the virus. The largest human epidemic occurred in Cape Province, South Africa, in 1974, when approximately 3,000 clinical cases of the virus were recorded.
The first recorded New World infection of West Nile Virus occurred during August 1999 in the borough of Queens, New York City. Through October 1999, 62 patients, 7 of whom died, had confirmed infections with the virus. Ornithophilic mosquitoes are the principal vectors of West Nile virus in the Old World. IN addition, the pattern of outbreaks in southern Europe suggests that viremic migratory birds may also contribute to movement of the virus. If so, West Nile virus has the potential to cause outbreaks throughout both temperate and tropical regions of the Western Hemisphere.
More than 4000 people were infected and 284 were killed by West Nile Virus (WVN) 20 states in 2002 in the United States, To date, WNV has been found in 44 states and the District of Columbia since it was first detected in the United States in 1999. WNV is a mosquito-borne flavivirus common in Africa, West Asia, and the Middle East. The virus can infect humans, birds, mosquitoes, horses, dogs, cats, and other mammals. WNV is closely related to viruses that cause St. Louis encephalitis, the most common mosquito-borne encephalitis in the United States, and Japanese encephalitis. WNV was first detected and isolated in the West Nile province of Uganda in 1937. The first recorded epidemic caused by WNV occurred in Israel during the early 1950s.
1. Butt Ca. Modern Study and Application of Chinese Materia Medica.
2. Subhuti Dharmananda PD. WEST NILE VIRUS. 2002.
3. CDC- Epidemiology Program [www.cvmvcd.org/information/ WNV%20Information/Document%205.pdf.
4. Harrington T KM, Kamel H, et al. West Nile Virus Infection Transmitted by Blood Transfusion. Transfusion. 2003;43:1018-1022.
5. West Nile Virus Activity -- United States, September 26-October 2, 2002, and Investigations of West Nile Virus Infections in Recipients of Blood Transfusion and Organ Transplantation. MMWR Morb Mortal Wkly Rep. 2002;51:884, 895.
6. None-noted. Investigation of Blood Transfusion Recipients With West Nile Virus Infections. MMWR Morb Mortal Wkly Rep. 2002;51:823.
7. None-noted. Investigations of West Nile Virus Infections in Recipients of Organ Transplantation and Blood Transfusion: Update. MMWR Morb Mortal Wkly Rep. 2002;51:833-836.
8. Investigations of West Nile Virus Infections in Recipients of Organ Transplantation and Blood Transfusion -- Michigan, 2002: Update. MMWR Morb Mortal Wkly Rep. 2002;51:879.
9. Iwamoto M JD, Guasch A, et al; West Nile Virus in Transplant Recipients Investigation Team. Transmission of West Nile Virus From an Organ Donor to Four Transplant Recipients. N Engl J Med. 2003;348:2196-2203.
10. Biggerstaff BJ PL. Estimated Risk of Transmission of the West Nile Virus Through Blood Transfusion in the US, 2002. Transfusion. 2003;43:1007-1017.
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