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Herpes simplex virus infections occur equally between the sexes throughout the year.
-Penn State Students in State College are at high risk when they touch lesions of herpes
HSV-1 transmission typically occurs via oral-oral, oral-genital, or genital-genital contact.
HSV-2 lesions largely involve the genital tract, with the virus remaining latent in the sacral nerve root ganglia (S2–S5)
Symptoms & Signs
Both viral subtypes can cause genital and oral–facial infections
The infections caused by the two subtypes are clinically indistinguishable.
Gingivostomatitis and pharyngitis: the most frequent clinical manifestations of primary HSV-1 infection; presents as small, grouped vesicles on an erythematous base, burning and stinging sensation, swollen and tender burning and stinging
Genital: most genital infections are caused by HSV-2; presents with bilateral genital ulcerations and tender lymphadenopathy.
Ocular disease: HSV keratitis presents with vision loss, pain, and discharge; it is a major cause of blindness from corneal scarring and opacity.
Neonatal & Congenital infection: Neonatal HSV can present as excessive tearing, eye pain, conjunctival edema, vesicular lesions of the mouth, palate, tongue, seizures, irritability, fever, multiple organ failure
CNS Disease: Both viruses can cause encephalitis; the temporal lobe is often involved; it presents with
the rapid onset of fever, headache, seizures, focal neurologic signs, and impaired consciousness
Bell’s Palsy: HSV-1 is a cause of Bell palsy (facial nerve paralysis)
Esophagitis & Proctitis: usually presents with dysphagia or odynophagia, fever, retrosternal chest pain
Erythema multiforme: HSV infection is the most common cause of EM; Cutaneous eruptions occur 2 to 7 days after herpes simplex infection
Diagnosis can be made by physical examination; Direct fluorescent antibody slide tests, viral culture, polymerase chain reaction
Early antiviral therapy within 72 hours of symptom onset
Antiviral drugs: Acyclovir, Famciclovir, Valacyclovir
Severe or frequent recurrences: Chronic suppressive therapy with antivirals
Keratitis: The usage of topical corticosteroids may exacerbate the infection
Male circumcision is associated with a lower incidence of acquiring HSV-2 infection.
Q. What is the most frequent sign of HSV reactivation disease? Herpes labialis
Q. What is the most frequent etiologic agent of Erythema multiforme? Herpes simplex virus
Q. What is the most common cause of fatal sporadic encephalitis in the United States? HSV-1 encephalitis
-Gilles de la Tourette syndrome is a chronic neuropsychiatric disorder characterized by multiple motor and phonic tics.
-Tics are sudden, involuntary, rapid, uncontrollable, repetitive, nonrhythmic, stereotyped movements with no purpose.
-Symptoms begin before 21 years of age, most often by the age of 11
-the course is one of remission and relapse.
-the disorder is more common in males than females
Symptoms & Signs
Tics typically start early, at 3–5 years of age, and peak around 9–12 years
Phonic Tics: Throat-clearing,gruting, barking, sniffing, hissing
Coprolalia: Vulgar or obscene speech
Echolalia: Parroting the speech of others
Echopraxia: Imitation of others’ movements
Palilalia: Repetition of words or phrases
Motor tics: Eye Blinking, facial grimacing, sniffing, hopping, jumping, and kicking, body gyrations, complex obscene gestures, neck jerking, shoulder shrugging
Sensory tics: Tics consisting of pressure, tickling, and warm or cold sensations
Behavioral disorders: Anxiety, obsessive-compulsive disorder, attention deficit disorder, depression
Diagnosis is made based on history and physical examination
Laboratory tests are normal
Behavioral therapy: Cognitive behavioral therapy, Habit reversal training
α-Adrenergic agonists: the first-line therapies
Clonidine: Most frequent side-effects are sedation, orthostatic hypotension, constipation
Antipsychotics: Risperidone, Aripiprazole,olanzapine, ziprasidone, Haloperidol, Pimozide
Botulinum toxin A injections
-the disorder is chronic, with waxing and waning
-Majority will experience significant improvement by the end of adolescence (80%).
-Restless legs syndrome is a chronic, neurological movement disorder characterized by a feeling of needing to move the legs (dysesthesia), associated with abnormal sensations like unpleasant creeping, crawling, tingling, and itching.
-Cause is unknown in most cases.
-Known causes of RLS: iron-deficiency anemia, renal failure, alcohol before sleep, thyroid disease, pregnancy, and certain medications
Anti-nausea drugs: Metoclopramide, Prochlorperazine
Anticonvulsants: Phenytoin, Droperidol
Antipsychotic drugs: Haloperidol
-The disorder seems especially common among pregnant women (1 in 5)
Symptoms & Signs
-Irresistible urge to move the limbs with creeping or crawling sensations
-Symptoms usually occur when patient is lying down or relaxing
-Abnormal sensations are temporarily alleviated by movement, stretching, or massage
-Symptoms are worse in the evening and first half of night
Diagnosis is usually made on clinical grounds alone
Search for iron deficiency: Ferritin levels should always be measured
– Stop aggravating medications, smoking, excessive alcohol consumption, coffee
-Daily moderate exercise, massage
-cognitive behavioral therapy
-RLS is treated by addressing the underlying cause
-Oral iron sulfate in patients with levels ≤ 75 mcg/L (13.4 mcmol/L)
-Other medications: Pramipexole, ropinirole, rotigotine, gabapentin, Pregabalin, Levodopa, clonazepam, temazepam, opiates
Dopaminergic therapy is the treatment of choice for severe cases but carries the risk of augmentation
Augmentation: the earlier onset or enhancement of symptoms; earlier onset of symptoms at rest; and a briefer response to medication.
RLS vs PLMS (Periodic Limb Movements of Sleep):
-RLS tends to occur during waking and at sleep onset, whereas PLMs occur during sleep.
-Patients with RLS sometimes also have PLMs, but patients with PLMs often do not have RLS.
Prognosis depends on the underlying cause
Q.Most common treatable cause of RLS: Iron deficiency
Q.What is the most common complication of long-term dopaminergic therapy? Augmentation
-Parkinson’s disease is a neurodegenerative disorder due to dopamine depletion in the substantia nigra and in the nigrostriatal pathway to the caudate and putamen.
-the second most common age-related neurodegenerative disease, exceeded only by Alzheimer’s disease (AD)
-The mean age of onset of PD is about 60 years
-The cause remains largely unknown
-The only known cause of PD: Genetic mutations
-Occurs in all ethnic groups with equal sex distribution
-Prior use of ibuprofen is associated with a decreased risk of developing Parkinson disease
Symptoms & Signs
rest tremor, rigidity (stiffness), bradykinesia (slowing), and gait dysfunction with postural instability. freezing of gait, speech difficulty, swallowing impairment, autonomic disturbances,
Cardinal features: Tremor (most conspicuous at rest, enhanced by stress)Rigidity, Bradykinesia(the most disabling symptom; a slowness of voluntary movement)
Craniofacial: Masked facial expression (hypomimia), hypophonia, Dysphagia, Repetition of a phrase or word with increasing rapidity (palilalia), speech impairment
Visual: blurred vision, Eyelid opening apraxia, hypometric saccades, impaired vestibuloocular reflex
Musculoskeletal: Stooped posture, micrographia, dystonia, myoclonus, difficulty turning in bed
Gait: A loss of the normal automatic arm swinging, Shuffling, Short-stepped gait, freezing, festination
Psychosis: Visual, auditory, olfactory, and tactile hallucinations
Olfactory dysfunction: loss of smell
Sensory disturbances: Pain
Mood disorders: Depression (most common psychiatric disturbance seen in PD), anxiety, loss of motivation,
Sleep disturbances: Rapid eye movement sleep behavior disorder (RBD), sleep fragmentation, early morning awakening, restless legs syndrome
Gastrointestinal disturbances Constipation, Dysphagia
Genitourinal disturbances Urinary difficulties
Sexual dysfunction: underactivity, hypersexuality
There are no diagnostic tests for PD
Primarily a clinical diagnosis based on symptoms and signs
Myerson Sign: Repetitive tapping (about twice per second) over the bridge of the nose producing a sustained blink response
Dopamine Replacement Therapy
Dopamine: Given the deficiency of dopamine, it would be nice if we could just give dopamine itself. However, dopamine does not cross the blood-brain barrier.
Logic behind Levodopa-Carbidopa combination:
Levodopa can cross the blood-brain barrier, but large doses are required because much of the drug is decarboxylated to dopamine in the periphery causing side-effects like nausea, vomiting, and orthostatic hypotension.
Carbidopa is a dopamine decarboxylase inhibitor that does not cross the blood–brain barrier. It reduces the peripheral metabolism of levodopa, thereby increasing the amount of levodopa that reaches the brain.
-It is the most effective symptomatic treatment for PD
-It controls classic motor features of PD, improves quality of life, and increases the lifespan
Selegiline, Rasagiline, Safinamide
At lower doses, Selegiline and rasagiline are not associated with a cheese effect (hypertensive crisis), usually seen when MAO-B inhibitors are taken with tyramine-rich containing foods
Side-effects: nausea, headache, confusion, hallucinations
-Tolcapone, Entacapone, Opicapone
-Inhibitors of COMT prolong the elimination half-life of levodopa and enhance its brain availability.
Side-effects of Tolcapone: Severe diarrhea, Fatal hepatic toxicity; periodic monitoring of liver function required
-Antiviral drug effective in the treatment of influenza
-it ameliorates dyskinesias resulting from prolonged levodopa therapy
-Side-effects: Livedo reticularis, weight gain; should always be discontinued gradually to prevent withdrawal-like symptoms
Dopamine Agonists (DAs)
Ergot DAs: Bromocriptine
Nonergot DAs: Pramipexole, Ropinirole, Rotigotine, Apomorphine
Due to their serious side-effects, the first generation dopamine agonists (bromocriptine, pergolide, cabergoline) were replaced by second generation agonists such as pramipexole, ropinirole, rotigotine.
-Side-effects: Sedation with sudden unintended episodes of falling asleep, impulse-control disorders (compulsive eating, shopping, hypersexuality, pathologic gambling)
Trihexyphenidyl(most widely prescribed anticholinergic), benztropine, biperiden
-Contraindicated in patients with prostatic hypertrophy, narrow-angle glaucoma, or obstructive intestinal disease
Side-effects: Dryness of the mouth, constipation, urinary retention, cardiac arrhythmias, palpitations, mydriasis, agitation, restlessness.
Olanzapine, Quetiapine, Risperidone, Clozapine
-Clozapine can cause marrow suppression, necessitating weekly cell counts
Antidepressants: selective serotonin-norepinephrine reuptake inhibitor (SNRI) or a selective serotonin reuptake inhibitor (SSRI), cognitive behavioral therapy
Stimulants: Modafinil, methylphenidate
Exercise and physical therapy
Cognitive behavioral therapy
Deep Brain Stimulation
The serum urate level may be a prognostic indicator in men—the rate of progression declines as the urate level increases.