TEMPOROMANDIBULAR JOINT (TMJ) SYNDROME - Scott A. Fields, MD
BASICS
DESCRIPTION
• Syndrome characterized by
- Pain and tenderness in jaw muscles
- Sound and/or pain over temporomandibular joint
- Limitation of mandibular movement
• System(s) Affected: Musculoskeletal
• Synonym(s): Myofascial pain-dysfunction syndrome
ALERT
Pregnancy Considerations
No association
GENERAL PREVENTION
• Elimination of tension-relieving oral habits
• Reduction in overall muscle tension
EPIDEMIOLOGY
• Predominant age: Symptoms more common age 30-50
• Predominant sex: Female > Male (3:1)
Prevalence
Symptoms or signs of TMJ dysfunction are present in up to 1/2 of the population, but only 5-25% seek treatment.
RISK FACTORS
• Chronic oral habit, such as clenching or grinding of the teeth
• Osteoarthritis, rheumatoid arthritis
• Dental malocclusion
• Fibrositis
• Psychosocial stress
ETIOLOGY
• TMJ synovitis
• TMJ disc derangement
• Hypermobile or hypomobile TMJ
• Occluso-muscular dysfunction (bruxism)
• Masticatory muscle spasm
• Trauma
• Poorly fitting dentures
ASSOCIATED CONDITIONS
Cranio-mandibular disorders
DIAGNOSIS
SIGNS AND SYMPTOMS
• Facial and/or TMJ pain
• Locking or catching of jaw
• TMJ noises: Clicking, grinding, popping
• Headache
• Earache
• Neck pain
Physical Exam
Jaw range of motion (opening, closing, lateral, protrusive) and masticatory muscle strength
TESTS
Imaging
• Single-contrast videoarthrography: Demonstrates joint dynamics and disc movement
• Panoramic dental radiographs
• MRI: Noninvasive study for disc position; information gained helps in deciding conservative versus surgical management
Pathological Findings
• Condylar head displacement
• Anterior disc displacement
• Posterior capsulitis
• Loosening of disc and capsular attachments
• Chondroid metaplasia of disc leading to disc perforation and degeneration
DIFFERENTIAL DIAGNOSIS
• Condylar fracture/dislocation
• Trigeminal neuralgia
• Dental or periodontal conditions
• TMJ neoplasm
TREATMENT
GENERAL MEASURES (1)[C]
• Jaw rest
• Local heat therapy
• Anti-inflammatory medications
• Muscle relaxants
• Analgesics
• Correction of malocclusion with orthodontic appliance
• Stress reduction
• Behavior modification to eliminate tension-relieving oral habits
• Buccal separator orthodontic appliance
• Linearly polarized, near-infrared irradiation
Diet
Soft diet to reduce chewing
MEDICATION (DRUGS)
First Line
• NSAIDs: No single drug more efficacious than another (1)[C]
• Botulinum toxin (2)[C]
• Contraindications
- History of anaphylaxis to aspirin
- Peptic ulcer disease
- Renal insufficiency
• Precautions
- Peptic ulcers, gastritis, or GI bleeding may occur with chronic use.
- May cause acute interstitial nephritis
- Drug accumulation with renal insufficiency
- Liver function abnormalities in up to 15% of patients
• Significant possible interactions
- Albumin-bound drugs: Displacement of either drug
- Warfarin: Increased prothrombin time
- Lithium: Increased lithium plasma level
- Furosemide: Decreased natriuretic effect
- Propranolol: Decreased antihypertensive effect
Second Line
• Analgesic agents (1)[C]
• Muscle relaxants (1)[C]
FOLLOW-UP
PROGNOSIS
• With conservative therapy, symptoms resolve in 3/4 of cases within 3 months.
• Patients benefit the most from a comprehensive treatment approach, including
- Correction of occlusal discrepancies
- Restoration of normal muscle function
- Pain control
- Stress management
- Behavior modification
COMPLICATIONS
• Secondary degenerative joint disease
• Chronic TMJ dislocation
• Loss of joint range of motion
• Depression and chronic pain syndromes
PATIENT MONITORING
• Ongoing assessment of clinical response to conservative therapies (NSAIDs, behavior modification, occlusal splints) is necessary.
• Surgical procedure to correct disc displacement or replace a damaged disc may be indicated only if the patient has not responded to conservative treatment.
REFERENCES
1. Laskin DM. Putting order into temporomandibular disorders. J Oral Maxillofac Surg. 1998;56:121.
2. Schwartz MB, Freund BB. Treatment of temporomandibular disorders with botulinum toxin. Clin J Pain. 2002;18(suppl 6):S198-S203.
3. Mock D. The differential diagnosis of temporomandibular joint disorders. J Orofac Pain. 1999;13:246-250.
4. Kuttila S, et al. Aural symptoms and signs of temporomandibular disorder in association with treatment need and visits to a physician. Laryngoscope. 1999;109:1669-1673.
5. Pankhurst CL. Controversies in the aetiology of temporomandibular disorders. Part 1. Temporomandibular disorders: All in the mind? Prim Dent Care. 1997;4:25-30.
6. Bush FM, Harkins SW, Harrington WG. Otalgia and aversive symptoms in temporomandibular disorders. Ann Otol Rhinol Laryngol. 1999;108:884-892.
7. Yokoyama K, Sugiyama K. Temporomandibular joint pain analgesia by linearly polarized near-infrared irradiation. Clin J Pain. 2001;17:47-51.
8. Dimitroulis G. The role of surgery in the management of disorders of the temporomandibular joint: A critical review of the literature. Part 1. Int J Oral Maxillofac Surg. 2004;33.
9. Dimitroulis G. The role of surgery in the management of disorders of the temporomandibular joint: A critical review of the literature. Part 2. Int J Oral Maxillofac Surg. 2005;34(3):231-237.
10. Al-Ani MZ, et al. Stabilisation splint therapy for temporomandibular pain dysfunction syndrome. Cochrane Oral Health Group Cochrane Database of Systematic Reviews. 1,2006.
11. Koh H, Robinson PG. Occlusal adjustment for treating and preventing temporomandibular joint disorders. Cochrane Oral Health Group Cochrane Database of Systematic Reviews. 1,2006.
MISCELLANEOUS
See also: Bruxism
Wednesday, January 7, 2009
TEETHING
TEETHING - Alan M. Ehrlich, MD
BASICS
DESCRIPTION
• Teething is the eruption of the deciduous teeth, which most children experience without difficulty. It is a natural, gradual, and predictable process, but the timetable varies from baby to baby.
• Deciduous teeth
- Most deciduous teeth begin to erupt at 5-7 months of age, and teething is completed by 2-3 years of age.
- The mandibular central incisors erupt 1st, then the 2 or 4 maxillary incisors, followed by the lower lateral incisors.
- After a few months, the 4 molars appear (the lower ones at 12 months of age, the upper ones at 14 months of age).
- After the cuspid teeth appear at 16-18 months of age, the 2nd molars erupt at 25-33 months of age.
- 25% normal babies may have delayed eruption of teeth until 4 or 6 teeth appear simultaneously after their 1st birthday.
- Premature babies erupt teeth according to their gestational age rather than their chronological age. If teething seems particularly delayed, refer patient to a pediatric dentist.
• Teeth in neonates
- 1 in 2,000 neonates are born with a tooth (appears to be familial).
- These neonatal teeth may be loose, but most are the normal deciduous lower central incisors and can persist.
- Mild ulceration in the sublingual area has been reported in 18% of these babies.
- Because of the potential for aspiration, there is some controversy about elective removal of the loose teeth (most pediatric dentists will remove these teeth if they are loose).
• System(s) Affected: Gastrointestinal
EPIDEMIOLOGY
Predominant age: Birth to 2 1/2 years of age
DIAGNOSIS
SIGNS AND SYMPTOMS
• A large percentage of babies have no signs or symptoms of teething.
• Excessive drooling and chewing on fingers begins at 3-4 months of age. This is also the time that normal hand-mouth stimulation increases salivation.
• Discomfort may be noted more with the eruption of the 1st tooth, the molars, and/or with the simultaneous eruption of multiple teeth.
• Restlessness, irritability, disturbed sleep, changes in feeding patterns, nasal discharge, mild cough, chin rash, fever, diarrhea, pulling of ear, and rubbing of the cheeks have been reported by parents. In any given infant, it is impossible to document that these are caused by teething, so parents and health providers should always consider other possible etiologies so as not to miss or delay diagnosing an illness.
History
• Biting
• Drooling
• Gum rubbing
• Sucking
• Irritability
• Wakefulness
• Ear rubbing
• Facial rash
• Decreased appetite for solid foods
Physical Exam
• A small red or white spot may appear over the swollen gum just prior to tooth eruption
• Local inflammation, swelling, and occasional hemorrhage can be found on the involved gums
DIFFERENTIAL DIAGNOSIS
Herpetic gingivostomatitis: Infants with fever, irritability, sleeplessness, and difficulty feeding may have underlying infection caused by herpes simplex virus. Some of these infants with positive culture may not have evidence of inflammation or ulceration expected in gingivitis.
TREATMENT
STABILIZATION
Outpatient
GENERAL MEASURES
• Treatment for teething includes reassurance for the parents and symptomatic relief, if needed.
• Provide the infant with a safe, 1-piece teething ring, clean cloth, or pacifier for gumming.
• Rub the involved swollen gums if the baby appears to be comforted by this.
• Cool fluids may be offered, but avoid frozen foods or objects. These could cause thermal damage to the tissues.
• Toast, cookies, bagels, and crackers are offered by some parents for teething, but parents must observe carefully to prevent choking.
• Avoid OTC preparations for teething such as lidocaine (Xylocaine 2%, Baby Ora-Gel, Num-zit Gel, Num-zit Liquid, Anbesol). Misuse, overuse, and sensitivity have been reported.
• Avoid the use of alcohol.
• For an infant with low-grade fever, irritability, and/or inflamed gums (where other comforting measures have not been of help), acetaminophen, in proper doses (10-15 mg/kg/dose q4h p.r.n.), can be used intermittently.
• Gum hematomas that erupt appear as blue cysts. Most do not require medical intervention. Be sure there are no other signs of a bleeding disorder.
• Breast-feeding babies may attempt to chew on the nipple at the end of sucking while teething but can be taught not to bite. Breast-feeding can continue after teeth are present.
• Advise parents to avoid sugared pacifiers, tying teething ring with cord around the infant's neck, and imported fluid-filled teething rings. They should remove painted furniture that may contain lead.
Diet
No special diet
Activity
No restrictions
MEDICATION (DRUGS)
First Line
Acetaminophen 10-15 mg/kg q4h as needed
FOLLOW-UP
PROGNOSIS
Normal progression through the teething process without illness
REFERENCES
1. Macknin ML, et al. Symptoms associated with infant teething. Pediatrics. 2000;105:747-752. [B]
2. Wake M et al. Teething and tooth eruption in infants. Pediatrics. 2000;106(6):1374-1379. [B]
3. Falkner F. Deciduous tooth eruption. Arch Dis Childhood. 1957;32:386-391.
4. Gardiner J. Erupted teeth in the newborn. Proc R Soc Med. 1961;4:504.
5. Golden N, Takieddine F, Hirsch V. Teething ageprematurely born infants. Am J Dis Child. 1981;135:903-904.
6. King DL, et al. Herpetic gingivostomatitis and teething difficulty in infants. Pediatr Dent. 1992;14:82-85.
7. King NM, Lee A. Prematurely erupted teeth in the newborn infant. J Pediatr. 1989;114:807.
8. McDonald RE. Eruption of the teeth, local, systematic and congenital factors that influence the process. In: Dentistry for the Child and Adolescent, 5th ed. St. Louis: Mosby; 1987:189-196.
9. Seward M. General disturbances attributed to the eruption of human primary dentition. J Dent Child. 1972;39:178-183.
ADDITIONAL READING
http://www.ada.org/public/topics/teething.asp
BASICS
DESCRIPTION
• Teething is the eruption of the deciduous teeth, which most children experience without difficulty. It is a natural, gradual, and predictable process, but the timetable varies from baby to baby.
• Deciduous teeth
- Most deciduous teeth begin to erupt at 5-7 months of age, and teething is completed by 2-3 years of age.
- The mandibular central incisors erupt 1st, then the 2 or 4 maxillary incisors, followed by the lower lateral incisors.
- After a few months, the 4 molars appear (the lower ones at 12 months of age, the upper ones at 14 months of age).
- After the cuspid teeth appear at 16-18 months of age, the 2nd molars erupt at 25-33 months of age.
- 25% normal babies may have delayed eruption of teeth until 4 or 6 teeth appear simultaneously after their 1st birthday.
- Premature babies erupt teeth according to their gestational age rather than their chronological age. If teething seems particularly delayed, refer patient to a pediatric dentist.
• Teeth in neonates
- 1 in 2,000 neonates are born with a tooth (appears to be familial).
- These neonatal teeth may be loose, but most are the normal deciduous lower central incisors and can persist.
- Mild ulceration in the sublingual area has been reported in 18% of these babies.
- Because of the potential for aspiration, there is some controversy about elective removal of the loose teeth (most pediatric dentists will remove these teeth if they are loose).
• System(s) Affected: Gastrointestinal
EPIDEMIOLOGY
Predominant age: Birth to 2 1/2 years of age
DIAGNOSIS
SIGNS AND SYMPTOMS
• A large percentage of babies have no signs or symptoms of teething.
• Excessive drooling and chewing on fingers begins at 3-4 months of age. This is also the time that normal hand-mouth stimulation increases salivation.
• Discomfort may be noted more with the eruption of the 1st tooth, the molars, and/or with the simultaneous eruption of multiple teeth.
• Restlessness, irritability, disturbed sleep, changes in feeding patterns, nasal discharge, mild cough, chin rash, fever, diarrhea, pulling of ear, and rubbing of the cheeks have been reported by parents. In any given infant, it is impossible to document that these are caused by teething, so parents and health providers should always consider other possible etiologies so as not to miss or delay diagnosing an illness.
History
• Biting
• Drooling
• Gum rubbing
• Sucking
• Irritability
• Wakefulness
• Ear rubbing
• Facial rash
• Decreased appetite for solid foods
Physical Exam
• A small red or white spot may appear over the swollen gum just prior to tooth eruption
• Local inflammation, swelling, and occasional hemorrhage can be found on the involved gums
DIFFERENTIAL DIAGNOSIS
Herpetic gingivostomatitis: Infants with fever, irritability, sleeplessness, and difficulty feeding may have underlying infection caused by herpes simplex virus. Some of these infants with positive culture may not have evidence of inflammation or ulceration expected in gingivitis.
TREATMENT
STABILIZATION
Outpatient
GENERAL MEASURES
• Treatment for teething includes reassurance for the parents and symptomatic relief, if needed.
• Provide the infant with a safe, 1-piece teething ring, clean cloth, or pacifier for gumming.
• Rub the involved swollen gums if the baby appears to be comforted by this.
• Cool fluids may be offered, but avoid frozen foods or objects. These could cause thermal damage to the tissues.
• Toast, cookies, bagels, and crackers are offered by some parents for teething, but parents must observe carefully to prevent choking.
• Avoid OTC preparations for teething such as lidocaine (Xylocaine 2%, Baby Ora-Gel, Num-zit Gel, Num-zit Liquid, Anbesol). Misuse, overuse, and sensitivity have been reported.
• Avoid the use of alcohol.
• For an infant with low-grade fever, irritability, and/or inflamed gums (where other comforting measures have not been of help), acetaminophen, in proper doses (10-15 mg/kg/dose q4h p.r.n.), can be used intermittently.
• Gum hematomas that erupt appear as blue cysts. Most do not require medical intervention. Be sure there are no other signs of a bleeding disorder.
• Breast-feeding babies may attempt to chew on the nipple at the end of sucking while teething but can be taught not to bite. Breast-feeding can continue after teeth are present.
• Advise parents to avoid sugared pacifiers, tying teething ring with cord around the infant's neck, and imported fluid-filled teething rings. They should remove painted furniture that may contain lead.
Diet
No special diet
Activity
No restrictions
MEDICATION (DRUGS)
First Line
Acetaminophen 10-15 mg/kg q4h as needed
FOLLOW-UP
PROGNOSIS
Normal progression through the teething process without illness
REFERENCES
1. Macknin ML, et al. Symptoms associated with infant teething. Pediatrics. 2000;105:747-752. [B]
2. Wake M et al. Teething and tooth eruption in infants. Pediatrics. 2000;106(6):1374-1379. [B]
3. Falkner F. Deciduous tooth eruption. Arch Dis Childhood. 1957;32:386-391.
4. Gardiner J. Erupted teeth in the newborn. Proc R Soc Med. 1961;4:504.
5. Golden N, Takieddine F, Hirsch V. Teething ageprematurely born infants. Am J Dis Child. 1981;135:903-904.
6. King DL, et al. Herpetic gingivostomatitis and teething difficulty in infants. Pediatr Dent. 1992;14:82-85.
7. King NM, Lee A. Prematurely erupted teeth in the newborn infant. J Pediatr. 1989;114:807.
8. McDonald RE. Eruption of the teeth, local, systematic and congenital factors that influence the process. In: Dentistry for the Child and Adolescent, 5th ed. St. Louis: Mosby; 1987:189-196.
9. Seward M. General disturbances attributed to the eruption of human primary dentition. J Dent Child. 1972;39:178-183.
ADDITIONAL READING
http://www.ada.org/public/topics/teething.asp
TARDIVE DYSKINESIA
TARDIVE DYSKINESIA - Lawrence E. Udom, MD, MPH
BASICS
DESCRIPTION
• Tardive dyskinesia (TD) is a neurologic syndrome that possesses the essential features of abnormal, involuntary movements of the tongue, lips, face, trunk, and extremities. It is most commonly associated with long-term treatment with neuroleptic medications. The movements can include grimacing, sticking out the tongue, and smacking and sucking the lips. They have choreiform characteristics (rapid, jerky, or nonrepetitive); athetoid characteristics (slow, sinuous, continual); or rhythmic characteristics. TD symptoms can begin during treatment with neuroleptics or within 4 weeks of discontinuing neuroleptics. TD can be mild, moderate, or severe.
• System(s) Affected: Nervous; Musculoskeletal
• Synonym(s): Orofacial dyskinesia
GENERAL PREVENTION
Choosing an "atypical" [newer] neuroleptic statistically makes the chance of TD less likely.
EPIDEMIOLOGY
• TD rates for patients beginning treatment with conventional antipsychotics in their 5th decade or later are 3 to 5 times those found for younger patients, despite treatment with lower doses. (1)
• Predominant age: Occurs in all ages; however, advanced age is a major risk factor for TD.
• Predominant sex: No difference in susceptibility between the genders until advanced years when females become more susceptible.
Incidence
In studies that used Haloperidol as their predominant classical antipsychotic
• Younger patients (55 years old) on the classical antipsychotics have a 5% incidence of developing TD per year of use with a 50-60% development over their lifetime.
• Older patients (>60 years old) had an approx. 20% incidence rate after 1 year of exposure, to 30%, and near 50% at 2- and 3-year exposures, respectively. (1)
Prevalence
There is overall estimated prevalence of 15-25% of TD within 5 years of continuous classical antipsychotic use.
RISK FACTORS
• Use of classical antipsychotics
- Haloperidol (Haldol)
- Chlorpromazine (Thorazine)
- Fluphenazine (Permitil, Prolixin)
- Thioridazine (Mellaril)
- Perphenazine (Trilafon)
- Trifluoperazine (Stelazine)
- Pimozide (Orap)
- Thiothixene (Navane)
- Molindone (Moban)
- A few of the new class of atypical antipsychotics have been linked to TD although in much lower incidences than noted with the older medications
Quetiapine (Seroquel)
Olanzapine (Zyprexa)
Risperidone (Risperdal)
• Length of neuroleptic use
• Older age
• Postmenopausal females
• Mental retardation
• Alcoholism and substance abuse
• Extrapyramidal symptoms early in the course of neuroleptic treatment
• Presence of other movement disorders
• Diabetes mellitus
• Mood disorders (particularly MDD)
ALERT
Geriatric Considerations
Occurs in all ages; however, advance age is a major risk factor for TD.
Genetics
No definitive data indicate a genetic basis for TD; however, recent research suggests a possible association with a polymorphic variant of the Ser9Gly DRD3 gene and severe TD. Also, the absence of a glutathione S-transferase gene (GSTM1) was associated with TD, particularly in white women. (2)
PATHOPHYSIOLOGY
The mechanism by which TD occurs is still under debate. Antipsychotics (both traditional and atypical) have a high affinity for the dopamine-2 (D2) receptors. It is postulated that the long-term blockade of these D2 receptors leads to an up-regulation in the number and sensitivity of D2 receptors in the striated region of the brain (which controls muscle coordination). This up-regulation is associated with involuntary movements and hence TD. It has also been postulated that the depletion of GABA in the substantia nigra may lead to orofacial dyskinesia, as may excess free radicals.
ETIOLOGY
Prolonged use of dopamine antagonist drugs, e.g.
• Traditional antipsychotics
• Atypical antipsychotics
• Metoclopramide (Reglan), an antiemetic with potent D2 antagonism
ASSOCIATED CONDITIONS
• Presence of movement disorder
• Psychiatric disorders commonly treated with neuroleptics
SIGNS AND SYMPTOMS
• Abnormal, involuntary movements of the tongue, lips, face, trunk, and extremities. In one major report
- 75% of individuals with TD have orofacial dyskinesia
- 50% have limb dyskinesia
- 25% have axial dyskinesia
- 10% have total body involvement
• Orofacial dyskinesia is common in the 60 years and older population
• Limb + axial dyskinesia is more common in the younger population. (3)
• These signs and symptoms must occur while taking neuroleptics or within 4 weeks or 8 weeks of withdrawal from an oral or depot neuroleptic medication, respectively.
• The signs typically begin minimal to mild in nature, and progress in severity with prolonged use.
History
• There must be a history of neuroleptic use for at least 3 months (or 1 month if individual's age is 60 years or older). TD must be distinguished from other movement disorders. The abnormal movements must not be due to a neurological condition or other general medical conditions (e.g., Huntington disease, Sydenham chorea, spontaneous dyskinesia, hyperthyroisim, heavy metal poisoning, Wilson disease), to ill-fitting dentures, or exposure to other medications that can cause acute reversible dyskinesia (l-dopa, bromocriptine, amantadine, Sinemet, Adderall, Ritalin, and Compazine). Other neuroleptic-induced movement disorders must be ruled out (e.g., tardive tourettism, blepharospasm, tardive akathisia, tardive myoclonus, tardive tremor, and tardive dystonia), as well as spontaneous dyskinesias and mental disorders.
• Question patient about a history of neurologic disorders that may involve the basal ganglia (e.g., cerebral vascular accident, encephalitis, head trauma, neoplasms).
• Attempt to illicit a family history for hereditary dyskinesias (e.g., Huntington disease).
• Ask about medication usage, particularly aforementioned medications.
- Note: Neuroleptics can also mask TD. Thus, the reason one may see onset after medication discontinuaton
Physical Exam
• Previously mentioned abnormal movements: Random movements in the tongue, lips, or jaw as well as facial grimacing; movements of arms, legs, fingers, and toes; or swaying movements of the trunk or hips
• See "Diagnosis" for possible rule out criteria
TESTS
There are several questionnaires created to illicit this information and rate TD on a severity scale; Most commonly used is the Abnormal Involuntary Movement Scale (AIMS) [A].
Lab
Only used to rule out other causes
Imaging
May be done to rule out other causes.
DIFFERENTIAL DIAGNOSIS
• Huntington disease
• Sydenham chorea
• Spontaneous dyskinesia
• Wilson disease
• Thyrotoxicosis
• Blepharospasm
• Tardive akathisia
• Tardive dystonia
• Physical signs may point the way to another diagnosis.
- Tachycardia, sweating, and a goiter suggests thyrotoxicosis.
- Jaundice, hepatomegaly, or Kayser-Fleischer rings suggest a work-up for Wilson disease.
• Dementia in addition to the movement disorder (chorea) and postural instability requires a workup for Huntington disease.
TREATMENT
STABILIZATION
Cessation of neuroleptic use
MEDICATION (DRUGS)
No definitive treatment for TD
• Replacement of traditional antipsychotic with an atypical (Risperidal, Olanzapine, Quetiapine, Ziprasidone, and Clozapine) (4)
• There has been some evidence that the use of Clozapine has been effective in diminishing involuntary movements in patients with TD. Some studies have shown remission of TD in up to 34% of cases after treatment with Clozapine. (5)[A] However, the side-effect of Clozapine (agranulocytosis) prevents it from being a first-line medication.
• Vitamin E, a free-radical scavenger, has been found in a number of studies to reduce the severity of TD. (6)[A] Supplementation seems to be most effective when started within the first 5 years of neuroleptic treatment. The most effective dosage is in question; one study reported that 1,600 IU of vitamin E per day may be the optimal amount (7,8)[B] but many studies have found this dose to be toxic. Therefore, vitamin E levels in patients must be monitored closely.
PROGNOSIS
TD can be mild to moderate with resolution of symptoms after a period of discontinuation from offending drug. There are rare incidences where TD may be severe and irreversible.
REFERENCES
1. Woerner MG, et al. Prospective study of tardive dyskinesia in the elderly: Rates and risk factors. Am J Psychiatry. 1998;155:1521-1528.
2. de Leon J, et al. Polymorphic variations in GSTM1, GSTT1, PgP, CYP2D6, CYP3A5, and dopamine D2 and D3 receptors and their association with tardive dyskinesia in severe mental illness. J Clin Psychopharmacol. 2005;25(5):448-456.
3. American Psychiatric Association. DSM-IV-TR 2000: Diagnostic Statistical Manual of Mental Disorders. 4th ed. American Psychiatric Publishing Inc; 2000.
4. Caroff SN, et al. Movement disorders associated with atypical antipsychotic drugs. J Clin Psychiatry. 2002;63(suppl 4):12-19.
5. Lieberman JA, et al. The effects of clozapine on tardive dyskinesia. Br J Psychiatry. 1191;158:503-510.
6. Adler LA, et al. Vitamin E treatment of tardive dyskinesia. Am J Psychiatry. 1993;150:1405-1407.
7. Hashim S, Sajjad A. Vitamin E in the treatment of tardive dyskinesia: A preliminary study over 7 months at different amounts. Int Clin Psychopharmacol 1988;13:147-155.
8. Egan MF, et al. Treatment of tardive dyskinesia with vitamin E. Am J Psychiatry. 1992;149:773-777.
ADDITIONAL READING
DSM-IV-TR
BASICS
DESCRIPTION
• Tardive dyskinesia (TD) is a neurologic syndrome that possesses the essential features of abnormal, involuntary movements of the tongue, lips, face, trunk, and extremities. It is most commonly associated with long-term treatment with neuroleptic medications. The movements can include grimacing, sticking out the tongue, and smacking and sucking the lips. They have choreiform characteristics (rapid, jerky, or nonrepetitive); athetoid characteristics (slow, sinuous, continual); or rhythmic characteristics. TD symptoms can begin during treatment with neuroleptics or within 4 weeks of discontinuing neuroleptics. TD can be mild, moderate, or severe.
• System(s) Affected: Nervous; Musculoskeletal
• Synonym(s): Orofacial dyskinesia
GENERAL PREVENTION
Choosing an "atypical" [newer] neuroleptic statistically makes the chance of TD less likely.
EPIDEMIOLOGY
• TD rates for patients beginning treatment with conventional antipsychotics in their 5th decade or later are 3 to 5 times those found for younger patients, despite treatment with lower doses. (1)
• Predominant age: Occurs in all ages; however, advanced age is a major risk factor for TD.
• Predominant sex: No difference in susceptibility between the genders until advanced years when females become more susceptible.
Incidence
In studies that used Haloperidol as their predominant classical antipsychotic
• Younger patients (55 years old) on the classical antipsychotics have a 5% incidence of developing TD per year of use with a 50-60% development over their lifetime.
• Older patients (>60 years old) had an approx. 20% incidence rate after 1 year of exposure, to 30%, and near 50% at 2- and 3-year exposures, respectively. (1)
Prevalence
There is overall estimated prevalence of 15-25% of TD within 5 years of continuous classical antipsychotic use.
RISK FACTORS
• Use of classical antipsychotics
- Haloperidol (Haldol)
- Chlorpromazine (Thorazine)
- Fluphenazine (Permitil, Prolixin)
- Thioridazine (Mellaril)
- Perphenazine (Trilafon)
- Trifluoperazine (Stelazine)
- Pimozide (Orap)
- Thiothixene (Navane)
- Molindone (Moban)
- A few of the new class of atypical antipsychotics have been linked to TD although in much lower incidences than noted with the older medications
Quetiapine (Seroquel)
Olanzapine (Zyprexa)
Risperidone (Risperdal)
• Length of neuroleptic use
• Older age
• Postmenopausal females
• Mental retardation
• Alcoholism and substance abuse
• Extrapyramidal symptoms early in the course of neuroleptic treatment
• Presence of other movement disorders
• Diabetes mellitus
• Mood disorders (particularly MDD)
ALERT
Geriatric Considerations
Occurs in all ages; however, advance age is a major risk factor for TD.
Genetics
No definitive data indicate a genetic basis for TD; however, recent research suggests a possible association with a polymorphic variant of the Ser9Gly DRD3 gene and severe TD. Also, the absence of a glutathione S-transferase gene (GSTM1) was associated with TD, particularly in white women. (2)
PATHOPHYSIOLOGY
The mechanism by which TD occurs is still under debate. Antipsychotics (both traditional and atypical) have a high affinity for the dopamine-2 (D2) receptors. It is postulated that the long-term blockade of these D2 receptors leads to an up-regulation in the number and sensitivity of D2 receptors in the striated region of the brain (which controls muscle coordination). This up-regulation is associated with involuntary movements and hence TD. It has also been postulated that the depletion of GABA in the substantia nigra may lead to orofacial dyskinesia, as may excess free radicals.
ETIOLOGY
Prolonged use of dopamine antagonist drugs, e.g.
• Traditional antipsychotics
• Atypical antipsychotics
• Metoclopramide (Reglan), an antiemetic with potent D2 antagonism
ASSOCIATED CONDITIONS
• Presence of movement disorder
• Psychiatric disorders commonly treated with neuroleptics
SIGNS AND SYMPTOMS
• Abnormal, involuntary movements of the tongue, lips, face, trunk, and extremities. In one major report
- 75% of individuals with TD have orofacial dyskinesia
- 50% have limb dyskinesia
- 25% have axial dyskinesia
- 10% have total body involvement
• Orofacial dyskinesia is common in the 60 years and older population
• Limb + axial dyskinesia is more common in the younger population. (3)
• These signs and symptoms must occur while taking neuroleptics or within 4 weeks or 8 weeks of withdrawal from an oral or depot neuroleptic medication, respectively.
• The signs typically begin minimal to mild in nature, and progress in severity with prolonged use.
History
• There must be a history of neuroleptic use for at least 3 months (or 1 month if individual's age is 60 years or older). TD must be distinguished from other movement disorders. The abnormal movements must not be due to a neurological condition or other general medical conditions (e.g., Huntington disease, Sydenham chorea, spontaneous dyskinesia, hyperthyroisim, heavy metal poisoning, Wilson disease), to ill-fitting dentures, or exposure to other medications that can cause acute reversible dyskinesia (l-dopa, bromocriptine, amantadine, Sinemet, Adderall, Ritalin, and Compazine). Other neuroleptic-induced movement disorders must be ruled out (e.g., tardive tourettism, blepharospasm, tardive akathisia, tardive myoclonus, tardive tremor, and tardive dystonia), as well as spontaneous dyskinesias and mental disorders.
• Question patient about a history of neurologic disorders that may involve the basal ganglia (e.g., cerebral vascular accident, encephalitis, head trauma, neoplasms).
• Attempt to illicit a family history for hereditary dyskinesias (e.g., Huntington disease).
• Ask about medication usage, particularly aforementioned medications.
- Note: Neuroleptics can also mask TD. Thus, the reason one may see onset after medication discontinuaton
Physical Exam
• Previously mentioned abnormal movements: Random movements in the tongue, lips, or jaw as well as facial grimacing; movements of arms, legs, fingers, and toes; or swaying movements of the trunk or hips
• See "Diagnosis" for possible rule out criteria
TESTS
There are several questionnaires created to illicit this information and rate TD on a severity scale; Most commonly used is the Abnormal Involuntary Movement Scale (AIMS) [A].
Lab
Only used to rule out other causes
Imaging
May be done to rule out other causes.
DIFFERENTIAL DIAGNOSIS
• Huntington disease
• Sydenham chorea
• Spontaneous dyskinesia
• Wilson disease
• Thyrotoxicosis
• Blepharospasm
• Tardive akathisia
• Tardive dystonia
• Physical signs may point the way to another diagnosis.
- Tachycardia, sweating, and a goiter suggests thyrotoxicosis.
- Jaundice, hepatomegaly, or Kayser-Fleischer rings suggest a work-up for Wilson disease.
• Dementia in addition to the movement disorder (chorea) and postural instability requires a workup for Huntington disease.
TREATMENT
STABILIZATION
Cessation of neuroleptic use
MEDICATION (DRUGS)
No definitive treatment for TD
• Replacement of traditional antipsychotic with an atypical (Risperidal, Olanzapine, Quetiapine, Ziprasidone, and Clozapine) (4)
• There has been some evidence that the use of Clozapine has been effective in diminishing involuntary movements in patients with TD. Some studies have shown remission of TD in up to 34% of cases after treatment with Clozapine. (5)[A] However, the side-effect of Clozapine (agranulocytosis) prevents it from being a first-line medication.
• Vitamin E, a free-radical scavenger, has been found in a number of studies to reduce the severity of TD. (6)[A] Supplementation seems to be most effective when started within the first 5 years of neuroleptic treatment. The most effective dosage is in question; one study reported that 1,600 IU of vitamin E per day may be the optimal amount (7,8)[B] but many studies have found this dose to be toxic. Therefore, vitamin E levels in patients must be monitored closely.
PROGNOSIS
TD can be mild to moderate with resolution of symptoms after a period of discontinuation from offending drug. There are rare incidences where TD may be severe and irreversible.
REFERENCES
1. Woerner MG, et al. Prospective study of tardive dyskinesia in the elderly: Rates and risk factors. Am J Psychiatry. 1998;155:1521-1528.
2. de Leon J, et al. Polymorphic variations in GSTM1, GSTT1, PgP, CYP2D6, CYP3A5, and dopamine D2 and D3 receptors and their association with tardive dyskinesia in severe mental illness. J Clin Psychopharmacol. 2005;25(5):448-456.
3. American Psychiatric Association. DSM-IV-TR 2000: Diagnostic Statistical Manual of Mental Disorders. 4th ed. American Psychiatric Publishing Inc; 2000.
4. Caroff SN, et al. Movement disorders associated with atypical antipsychotic drugs. J Clin Psychiatry. 2002;63(suppl 4):12-19.
5. Lieberman JA, et al. The effects of clozapine on tardive dyskinesia. Br J Psychiatry. 1191;158:503-510.
6. Adler LA, et al. Vitamin E treatment of tardive dyskinesia. Am J Psychiatry. 1993;150:1405-1407.
7. Hashim S, Sajjad A. Vitamin E in the treatment of tardive dyskinesia: A preliminary study over 7 months at different amounts. Int Clin Psychopharmacol 1988;13:147-155.
8. Egan MF, et al. Treatment of tardive dyskinesia with vitamin E. Am J Psychiatry. 1992;149:773-777.
ADDITIONAL READING
DSM-IV-TR
TAPEWORM INFESTATION
TAPEWORM INFESTATION - Kenton Voorhees, MD, FAAFP
BASICS
DESCRIPTION
• Tapeworms (cestodes, flatworms) can be parasitic in humans.
• Adult worms consist of a head (scolex), which attaches to the host's gastrointestinal (GI) tract; a neck; and a segmented body (strobila), with individual segments (proglottid) containing sets of male and female reproductive organs that produce eggs.
• The life cycle of all but Hymenolepis nana requires an intermediate host, where they grow as larval forms in tissue that is then ingested by the final host, where it subsequently develops into an adult. H. nana can complete all stages of development in humans, helping to make it the most common tapeworm in humans.
• Most tapeworm infections are confined to the GI tract, except in Taenia solium (causing cysticercosis), or with Echinococcus infections, making infections with these more serious.
• Neurocysticercosis is the most common inpatient disorder due to parasite infection.
• Common tapeworms and their usual intermediate hosts and type of infection in humans include
Tapeworm intermediate hosts
Name Host D. latum Freshwater fish D. caninum Dog, cat, fleas E. granulosis Human, sheep, cow, dog E. multilocularis Fox, coyotes, cats, rodents H. diminuta Rodent, insects H. nana Human, rodent, insects T. saginata Cow T. solium Pig
• Taenia saginata: Beef causing an intestinal worm; 2-4 months from ingestion to adult; 3-10 m long; usually single tapeworm. Proglottids are motile; may crawl out of anus. May live 30 years
• Taenia solium: Pork; Intestinal worm or cysticercosis 2-4 months to become adult worm; 3 m long, occasionally multiple. Proglottids not motile. May live up to 25 years. Ingestion of encysted larvae (cysticerci) causes intestinal tapeworm. Ingestion of T. solium eggs causes cysticercosis. Eggs look identical to T. saginata eggs.
• Diphyllobothrium latum and other species: Freshwater fish; Intestinal worm. Longest adult tapewormup to 25 m. Matures to adult in 3-5 weeks
• H. nana: Rodent, insects, or humans; intestinal worm. Mature to adult worms in 10-12 days. Seldom exceeds 40 mm long. Proglottids rarely seen in stool. Eggs can autoinfect individual, or occasionally insects (especially meal worms). Fecal-oral transmission possible. Life span 4-10 weeks, but autoinfection can perpetuate infection. Usually self-cleared by adolescence
• Echinococcus granulosis and E. multilocularis: Humans, sheep, and cattle are intermediate hosts, with dogs the definitive hosts for E. granulosis. Foxes, coyotes, or cats are definitive hosts for E. multilocularis, with rodents the intermediate hosts. E. granulosiscystic Echinococcus. E. multilocularisalveolar Echinococcus. Hydatid disease of liver, spleen, etc., or alveolar hydatid disease Adult worm lives in dogs (or rodents). Human ingests eggs; larvae hatch and are carried through circulation to various organs such as liver and lungs, where they develop into hydatid cysts that enlarge, causing symptoms perhaps 5-20 years later.
• H. diminuta: Rodents and insects; intestinal worm. 90 cm long. Humans rare accidental hosts, by swallowing mealworms or grain beetles from grain.
• Dipylidium caninum: Dogs and cats, and fleas; intestinal worm. 10-70 cm long. Motile proglottids, shape of cucumber seeds, can crawl out anus. Rare accidental infection by ingesting infected flea that came from dogs or cats
• System(s) Affected: Gastrointestinal; Nervous
ALERT
Pediatric Considerations
• H. nana, highest among children with fecal-oral spread
• H. diminuta and D. caninum more common in children, as more likely to ingest insects accidentally
GENERAL PREVENTION
• Treatment of infected animals, populations, and screening household contacts, immigrants
• Improved sewage treatment
• See Patient Teaching
EPIDEMIOLOGY
• Predominant age: All ages affected
- H. nana and H. diminuta more common in children
• Predominant sex: Male = Female
Incidence
• Occurs infrequently
• More often associated with immigrant populations with cultural eating habits
• Can be endemic when fecal contamination enters water or food supplies
RISK FACTORS
• Taenias: Eating raw beef or pork, particularly in Africa, Central America, Asia
• Cysticercosis: A tapeworm carrier in close environment. Water contaminated with sewage
• Diphyllobothrium: Eating raw or undercooked fish, particularly in northern Europe
• H. nana: More frequent in children, the institutionalized, malnourished, and immunodeficient
• E. granulosis: Keeping dogs around sheep and goats; highest risk for hydatid cyst disease
• E. multilocularis: Contact with foxes, coyotes; mostly found in northern latitudes
ETIOLOGY
Eating the infective form of the parasite, either by eating contaminated food (meat, fish) or infected insects in cereals or grains, or through fecal-oral contamination
DIAGNOSIS
SIGNS AND SYMPTOMS
• T. saginata (beef tapeworm): Often noted by passing eggs or proglottids, which can be felt crawling out of anus. Mild gastrointestinal symptoms may occur: Nausea, abdominal pain, change in appetite, weakness, weight loss, allergic symptoms, urticaria, pruritus
• T. solium (pork tapeworm): Intestinal wormnoted passing eggs or proglottids. Occasional minor abdominal complaints similar to T. saginata. Larval migrationcysticercosismost common to brain and skeletal muscle. Neurologic manifestations such as new onset of seizures, focal neurologic deficits, hydrocephalus, headache, vomiting, visual changes, dizziness
• D. latum (fish tapeworm): Noted passing eggs, or proglottid segments or vomiting segment of worm. Occasionally mild abdominal discomfort, weight loss. Worm has marked affinity for vitamin B12; 40% decreased B12 levels, 2% megaloblastic anemia with glossitis
• H. nana (dwarf tapeworm): Anorexia, abdominal pain, and diarrhea
• Echinococcosis (hydatid disease): E. granulosis often asymptomatic for years. Liver cystsabdominal pain, right upper quadrant mass, obstructive jaundice. Cyst rupturefever, urticaria, pruritus, anaphylaxis. Pulmonary cystcough, chest pain, hemoptysis. Other organs possiblebone with pathologic fractures, CNS, cardiac conduction defects, pericarditis
• H. diminuta (rodent tapeworm): Pass eggs in stool, proglottids disintegrate. Headache, mild GI symptomsanorexia, nausea, cramps, diarrhea
• D. caninum (dog tapeworm): Occasionally abdominal pain, diarrhea, anal pruritus, urticaria. May observe proglottid in diaper or stool
TESTS
• Stool evaluation of ova and parasites
• Microscopic evaluation of proglottid collected in water or saline
• Antibody testing by ELISA to differentiate T. saginata eggs from T. solium
• Enzyme-linked immunoelectrotransfer blot: Test of choice for cysticercosis, Echinococcus (1)[C]
• DNA probes for T. saginata or T. solium
Lab
• Mild to moderate eosinophilia, increased IgE
• Microscopic analysis of eggs or proglottids
• Macrocytic, megaloblastic anemia rarely with diphyllobothriasis
Imaging
• Intestinal tapeworms occasionally seen by small bowel enteroclysis
• Cysticercosis: MRI preferred, CT OK (1)[C]
• Echinococcus cysts: Start with ultrasound
Diagnostic Procedures/Surgery
• Excisional biopsy of cysticercosis cyst
• Perianal inspection for eggs or proglottids
Pathological Findings
• Intestinal tapeworms: No pathologic findings
• Cysticercosis: Cysts, 5-10 mm in soft tissue. Calcified cysts in CNS, muscle
• Echinococcus: Hydatid cyst in liver, lung, other
DIFFERENTIAL DIAGNOSIS
• Nontapeworm gastroenteritis
• Irritable bowel syndrome
• Intestinal obstruction
• Cholecystitis or biliary obstruction
• B12 deficiency from nontapeworm etiologies
• Tumors (abscesses, malignant, benign)
• Idiopathic epilepsy
TREATMENT
Outpatient unless complications from cysts
GENERAL MEASURES
• Treatment of population in endemic area
• Treatment of all immigrants from endemic countries with albendazole is being evaluated.
• General supportive care during treatment
• Good hygienic measures should be employed.
• Asymptomatic cysticercosis may resolve spontaneously without treatment; however, antiparasitic therapy of parenchymal cysts may reduce the number of seizures with generalization. Treatment may induce an inflammatory response and symptoms. (2)[C]
Diet
As tolerated
Activity
As tolerated
MEDICATION (DRUGS)
First Line
• Praziquantel (Droncit): (1,3,4)[C]
- Single dose of 5-10 mg/kg (generally 10 mg/kg) for taeniasis, diphyllobothriasis, dipylidium infection, and most other intestinal cestodes (cure rate >95%)
- Single dose of 25 mg/kg for H. nana adults or children (cure rate >95%)
- 50-100 mg/kg/d t.i.d. 14-30 days for children and adults for cysticercosis
• Albendazole (Zentel): (1,3,4)[C]
- Dose: Weight >60 kg, 400 mg b.i.d. with meals; weight 60 kg, 15 mg/kg/d b.i.d. (maximum 800 mg/d)
- For Echinococcus hydatid cysts, give for 28 days, 14 days off, repeat for 3 cycles; can be 1-6 months
- For neurocysticercosis, drug of choice, give for 8-30 days, but examine for retinal lesions first; may repeat
• Neurocysticercosis: Steroids, anticonvulsants. Dexamethasone 4.5-12 mg/d (4)[C]
• PAIR therapy (puncture, aspiration, injection of a scolicidal, reaspiration) compares favorably with surgery for cystic echinococcosis.
• Contraindications
- Prior sensitivity
• Precautions
- Niclosamide: Occasional nausea and abdominal pain, diarrhea, dizziness
- Praziquantel: Mild but frequent dizziness, myalgias, nausea, diarrhea, abdominal pain
- Albendazole: Diarrhea and abdominal pain; leukopenia, increased transaminase levels
• Significant possible interactions
- Phenytoin and carbamazepine can induce metabolism of praziquantel by cytochrome P-450, causing treatment failure.
- Cimetidine, dexamethasone, and praziquantel can increase concentration of albendazole.
- Corticosteroids may decrease concentration of praziquantel.
Second Line
Niclosamide (Nicloside) (not available in the United States)
• Single dose of 2 g for adult or 50 mg/kg for children for diphyllobothriasis, taeniasis, and dipylidium infection (cure rate 90% for taeniasis and slightly less for diphyllobothriasis)
• 2 g, then 1 g/d for 5 more days for H. nana
SURGERY
• Cysticercosis and hydatid cysts have been removed surgically, with care not to leak fluid.
- Shunts for hydrocephalus (4)[C]
• Echinococcus hydatid cysts: (5)[C]
- Surgery based upon location of cyst
- Surgical risks may make medical therapy preferred.
- Surgery generally involves total pericystectomy or partial resection of the affected organ, with albendazole pretreatment for 1 month.
- Follow surgery with albendazole.
FOLLOW-UP
PROGNOSIS
• Cure of >95% of intestinal tapeworms with medications
• H. nana often self-cured by adolescence
• E. multilocularis often severe or fatal
• Prognosis of systemic cysts by location
• NeurocysticercosisIntraparenchymal cysts often benign. Extraparenchymal (subarachnoid, ventricular, cisternal) more serious (1)[C]
COMPLICATIONS
• Larval form of T. solium can cause system-wide cysticercosis, including neurocysticercosis (etiologic in up to 25% of cases of new-onset seizures in indigenous areas).
• Echinococcus hydatid cysts may cause abnormalities in the organ involved. Cyst rupture can cause spread of disease and anaphylaxis.
• B12 deficiency with D. latum
• Proglottid of T. saginata can rarely obstruct appendix and pancreatic and bile ducts.
• D. latum can occasionally cause intestinal obstruction, cholangitis, and cholecystitis.
PATIENT MONITORING
• Examine several stool specimens for ova and parasites at 3 months for Taenia species and 1 month for others.
• Follow neurocysticercosis with CT.
REFERENCES
1. Garcia HH, et al. Diagnosis, treatment and control of Taenia solium cysticercosis. Curr Opin Infect Dis. 2003;16:411-419.
2. Garcia HH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. 2004;350:249-258.
3. Abramowicz M, ed. The Medical Letter on Drugs and Therapeutics. Drugs for Parasitic Infections. New Rochelle, NY: The Medical Letter; August, 2004.
4. Garcia HH, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. 2002;15(4):747-756.
5. Guidelines for treatment of cystic and alveolar echinococcosis in humans. WHO Informal Working Group on Echinococcosis. Bull World Health Organ. 1996;74:231-242.
BASICS
DESCRIPTION
• Tapeworms (cestodes, flatworms) can be parasitic in humans.
• Adult worms consist of a head (scolex), which attaches to the host's gastrointestinal (GI) tract; a neck; and a segmented body (strobila), with individual segments (proglottid) containing sets of male and female reproductive organs that produce eggs.
• The life cycle of all but Hymenolepis nana requires an intermediate host, where they grow as larval forms in tissue that is then ingested by the final host, where it subsequently develops into an adult. H. nana can complete all stages of development in humans, helping to make it the most common tapeworm in humans.
• Most tapeworm infections are confined to the GI tract, except in Taenia solium (causing cysticercosis), or with Echinococcus infections, making infections with these more serious.
• Neurocysticercosis is the most common inpatient disorder due to parasite infection.
• Common tapeworms and their usual intermediate hosts and type of infection in humans include
Tapeworm intermediate hosts
Name Host D. latum Freshwater fish D. caninum Dog, cat, fleas E. granulosis Human, sheep, cow, dog E. multilocularis Fox, coyotes, cats, rodents H. diminuta Rodent, insects H. nana Human, rodent, insects T. saginata Cow T. solium Pig
• Taenia saginata: Beef causing an intestinal worm; 2-4 months from ingestion to adult; 3-10 m long; usually single tapeworm. Proglottids are motile; may crawl out of anus. May live 30 years
• Taenia solium: Pork; Intestinal worm or cysticercosis 2-4 months to become adult worm; 3 m long, occasionally multiple. Proglottids not motile. May live up to 25 years. Ingestion of encysted larvae (cysticerci) causes intestinal tapeworm. Ingestion of T. solium eggs causes cysticercosis. Eggs look identical to T. saginata eggs.
• Diphyllobothrium latum and other species: Freshwater fish; Intestinal worm. Longest adult tapewormup to 25 m. Matures to adult in 3-5 weeks
• H. nana: Rodent, insects, or humans; intestinal worm. Mature to adult worms in 10-12 days. Seldom exceeds 40 mm long. Proglottids rarely seen in stool. Eggs can autoinfect individual, or occasionally insects (especially meal worms). Fecal-oral transmission possible. Life span 4-10 weeks, but autoinfection can perpetuate infection. Usually self-cleared by adolescence
• Echinococcus granulosis and E. multilocularis: Humans, sheep, and cattle are intermediate hosts, with dogs the definitive hosts for E. granulosis. Foxes, coyotes, or cats are definitive hosts for E. multilocularis, with rodents the intermediate hosts. E. granulosiscystic Echinococcus. E. multilocularisalveolar Echinococcus. Hydatid disease of liver, spleen, etc., or alveolar hydatid disease Adult worm lives in dogs (or rodents). Human ingests eggs; larvae hatch and are carried through circulation to various organs such as liver and lungs, where they develop into hydatid cysts that enlarge, causing symptoms perhaps 5-20 years later.
• H. diminuta: Rodents and insects; intestinal worm. 90 cm long. Humans rare accidental hosts, by swallowing mealworms or grain beetles from grain.
• Dipylidium caninum: Dogs and cats, and fleas; intestinal worm. 10-70 cm long. Motile proglottids, shape of cucumber seeds, can crawl out anus. Rare accidental infection by ingesting infected flea that came from dogs or cats
• System(s) Affected: Gastrointestinal; Nervous
ALERT
Pediatric Considerations
• H. nana, highest among children with fecal-oral spread
• H. diminuta and D. caninum more common in children, as more likely to ingest insects accidentally
GENERAL PREVENTION
• Treatment of infected animals, populations, and screening household contacts, immigrants
• Improved sewage treatment
• See Patient Teaching
EPIDEMIOLOGY
• Predominant age: All ages affected
- H. nana and H. diminuta more common in children
• Predominant sex: Male = Female
Incidence
• Occurs infrequently
• More often associated with immigrant populations with cultural eating habits
• Can be endemic when fecal contamination enters water or food supplies
RISK FACTORS
• Taenias: Eating raw beef or pork, particularly in Africa, Central America, Asia
• Cysticercosis: A tapeworm carrier in close environment. Water contaminated with sewage
• Diphyllobothrium: Eating raw or undercooked fish, particularly in northern Europe
• H. nana: More frequent in children, the institutionalized, malnourished, and immunodeficient
• E. granulosis: Keeping dogs around sheep and goats; highest risk for hydatid cyst disease
• E. multilocularis: Contact with foxes, coyotes; mostly found in northern latitudes
ETIOLOGY
Eating the infective form of the parasite, either by eating contaminated food (meat, fish) or infected insects in cereals or grains, or through fecal-oral contamination
DIAGNOSIS
SIGNS AND SYMPTOMS
• T. saginata (beef tapeworm): Often noted by passing eggs or proglottids, which can be felt crawling out of anus. Mild gastrointestinal symptoms may occur: Nausea, abdominal pain, change in appetite, weakness, weight loss, allergic symptoms, urticaria, pruritus
• T. solium (pork tapeworm): Intestinal wormnoted passing eggs or proglottids. Occasional minor abdominal complaints similar to T. saginata. Larval migrationcysticercosismost common to brain and skeletal muscle. Neurologic manifestations such as new onset of seizures, focal neurologic deficits, hydrocephalus, headache, vomiting, visual changes, dizziness
• D. latum (fish tapeworm): Noted passing eggs, or proglottid segments or vomiting segment of worm. Occasionally mild abdominal discomfort, weight loss. Worm has marked affinity for vitamin B12; 40% decreased B12 levels, 2% megaloblastic anemia with glossitis
• H. nana (dwarf tapeworm): Anorexia, abdominal pain, and diarrhea
• Echinococcosis (hydatid disease): E. granulosis often asymptomatic for years. Liver cystsabdominal pain, right upper quadrant mass, obstructive jaundice. Cyst rupturefever, urticaria, pruritus, anaphylaxis. Pulmonary cystcough, chest pain, hemoptysis. Other organs possiblebone with pathologic fractures, CNS, cardiac conduction defects, pericarditis
• H. diminuta (rodent tapeworm): Pass eggs in stool, proglottids disintegrate. Headache, mild GI symptomsanorexia, nausea, cramps, diarrhea
• D. caninum (dog tapeworm): Occasionally abdominal pain, diarrhea, anal pruritus, urticaria. May observe proglottid in diaper or stool
TESTS
• Stool evaluation of ova and parasites
• Microscopic evaluation of proglottid collected in water or saline
• Antibody testing by ELISA to differentiate T. saginata eggs from T. solium
• Enzyme-linked immunoelectrotransfer blot: Test of choice for cysticercosis, Echinococcus (1)[C]
• DNA probes for T. saginata or T. solium
Lab
• Mild to moderate eosinophilia, increased IgE
• Microscopic analysis of eggs or proglottids
• Macrocytic, megaloblastic anemia rarely with diphyllobothriasis
Imaging
• Intestinal tapeworms occasionally seen by small bowel enteroclysis
• Cysticercosis: MRI preferred, CT OK (1)[C]
• Echinococcus cysts: Start with ultrasound
Diagnostic Procedures/Surgery
• Excisional biopsy of cysticercosis cyst
• Perianal inspection for eggs or proglottids
Pathological Findings
• Intestinal tapeworms: No pathologic findings
• Cysticercosis: Cysts, 5-10 mm in soft tissue. Calcified cysts in CNS, muscle
• Echinococcus: Hydatid cyst in liver, lung, other
DIFFERENTIAL DIAGNOSIS
• Nontapeworm gastroenteritis
• Irritable bowel syndrome
• Intestinal obstruction
• Cholecystitis or biliary obstruction
• B12 deficiency from nontapeworm etiologies
• Tumors (abscesses, malignant, benign)
• Idiopathic epilepsy
TREATMENT
Outpatient unless complications from cysts
GENERAL MEASURES
• Treatment of population in endemic area
• Treatment of all immigrants from endemic countries with albendazole is being evaluated.
• General supportive care during treatment
• Good hygienic measures should be employed.
• Asymptomatic cysticercosis may resolve spontaneously without treatment; however, antiparasitic therapy of parenchymal cysts may reduce the number of seizures with generalization. Treatment may induce an inflammatory response and symptoms. (2)[C]
Diet
As tolerated
Activity
As tolerated
MEDICATION (DRUGS)
First Line
• Praziquantel (Droncit): (1,3,4)[C]
- Single dose of 5-10 mg/kg (generally 10 mg/kg) for taeniasis, diphyllobothriasis, dipylidium infection, and most other intestinal cestodes (cure rate >95%)
- Single dose of 25 mg/kg for H. nana adults or children (cure rate >95%)
- 50-100 mg/kg/d t.i.d. 14-30 days for children and adults for cysticercosis
• Albendazole (Zentel): (1,3,4)[C]
- Dose: Weight >60 kg, 400 mg b.i.d. with meals; weight 60 kg, 15 mg/kg/d b.i.d. (maximum 800 mg/d)
- For Echinococcus hydatid cysts, give for 28 days, 14 days off, repeat for 3 cycles; can be 1-6 months
- For neurocysticercosis, drug of choice, give for 8-30 days, but examine for retinal lesions first; may repeat
• Neurocysticercosis: Steroids, anticonvulsants. Dexamethasone 4.5-12 mg/d (4)[C]
• PAIR therapy (puncture, aspiration, injection of a scolicidal, reaspiration) compares favorably with surgery for cystic echinococcosis.
• Contraindications
- Prior sensitivity
• Precautions
- Niclosamide: Occasional nausea and abdominal pain, diarrhea, dizziness
- Praziquantel: Mild but frequent dizziness, myalgias, nausea, diarrhea, abdominal pain
- Albendazole: Diarrhea and abdominal pain; leukopenia, increased transaminase levels
• Significant possible interactions
- Phenytoin and carbamazepine can induce metabolism of praziquantel by cytochrome P-450, causing treatment failure.
- Cimetidine, dexamethasone, and praziquantel can increase concentration of albendazole.
- Corticosteroids may decrease concentration of praziquantel.
Second Line
Niclosamide (Nicloside) (not available in the United States)
• Single dose of 2 g for adult or 50 mg/kg for children for diphyllobothriasis, taeniasis, and dipylidium infection (cure rate 90% for taeniasis and slightly less for diphyllobothriasis)
• 2 g, then 1 g/d for 5 more days for H. nana
SURGERY
• Cysticercosis and hydatid cysts have been removed surgically, with care not to leak fluid.
- Shunts for hydrocephalus (4)[C]
• Echinococcus hydatid cysts: (5)[C]
- Surgery based upon location of cyst
- Surgical risks may make medical therapy preferred.
- Surgery generally involves total pericystectomy or partial resection of the affected organ, with albendazole pretreatment for 1 month.
- Follow surgery with albendazole.
FOLLOW-UP
PROGNOSIS
• Cure of >95% of intestinal tapeworms with medications
• H. nana often self-cured by adolescence
• E. multilocularis often severe or fatal
• Prognosis of systemic cysts by location
• NeurocysticercosisIntraparenchymal cysts often benign. Extraparenchymal (subarachnoid, ventricular, cisternal) more serious (1)[C]
COMPLICATIONS
• Larval form of T. solium can cause system-wide cysticercosis, including neurocysticercosis (etiologic in up to 25% of cases of new-onset seizures in indigenous areas).
• Echinococcus hydatid cysts may cause abnormalities in the organ involved. Cyst rupture can cause spread of disease and anaphylaxis.
• B12 deficiency with D. latum
• Proglottid of T. saginata can rarely obstruct appendix and pancreatic and bile ducts.
• D. latum can occasionally cause intestinal obstruction, cholangitis, and cholecystitis.
PATIENT MONITORING
• Examine several stool specimens for ova and parasites at 3 months for Taenia species and 1 month for others.
• Follow neurocysticercosis with CT.
REFERENCES
1. Garcia HH, et al. Diagnosis, treatment and control of Taenia solium cysticercosis. Curr Opin Infect Dis. 2003;16:411-419.
2. Garcia HH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. 2004;350:249-258.
3. Abramowicz M, ed. The Medical Letter on Drugs and Therapeutics. Drugs for Parasitic Infections. New Rochelle, NY: The Medical Letter; August, 2004.
4. Garcia HH, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. 2002;15(4):747-756.
5. Guidelines for treatment of cystic and alveolar echinococcosis in humans. WHO Informal Working Group on Echinococcosis. Bull World Health Organ. 1996;74:231-242.
