Profofol Infusion syndrome

This patient fulfills the clinical criteria for propofol infusion syndrome. The clinical features of propofol
infusion syndrome are acute refractory bradycardia leading to asystole, in the presence of one or more
of the following: metabolic acidosis (base deficit > 10 mmol/l, rhabdomyolysis, hyperlipidemia, and
enlarged or fatty liver. There is an association between propofol infusion syndrome and propofol
infusions at doses higher than 4 m/kg/hour for greater than 48 hours. An early sign of cardiac instability
associated with propofol infusion syndrome is the development of right bundle branch block with
convex-curved ('coved type') ST elevation in the right praecordial leads (V1 to V3) of the
electrocardiogram

PCP/parkinon/Lewy body dementia

This patient has clinical manifestations of parkinsonism with bradykinesia, postural instability, and
rigidity. However, this patient also has additional manifestations included impaired voluntary eye
movements, with an intact oculocephalic reflex. This presentation is most consistent with progressive
supra nuclear palsy, which is pathologically characterized by tau inclusions in the substantial nigra.
Alpha-synuclein inclusions are seen in the substantial nigra in Parkinson disease and in cortical neurons
in Dementia with Lewy Bodies

Ataxia Telangiectasia

Ataxia telangiectasia (AT) is characterized by progressive cerebellar ataxia, oculocutaneous

telangiectasia, progressive cerebellar dysfunction, and recurrent sinopulmonary infections secondary to
progressive immunological and neurologic dysfunction. AT patients are significantly predisposed to
cancer, particularly lymphomas and leukemia. Other manifestations of the disease include sensitivity to
ionizing radiation, premature aging, and hypogonadism. AT has been a major interest of scientists since
the 78 1960's because it may yield an insight into numerous other major health problems, such as
cancer, neurologic disease, immunodeficiency, and aging. AT is characterized by: early-onset progressive
cerebellar ataxia, oculocutaneous telangiectasia (dilated blood vessels in the eyes and skin),
immunodeficiency mostly thorough lowering of IgA, IgG and IgE levels, chromosomal instability,
hypersensitivity to ionizing radiation, increased incidence of malignancies primarily lymphoid, and raised
alpha-fetoprotein levels.

Medication overuse headahe

The risk of developing medication overuse headache is highest with butalbital (5 days of use per month),
followed by opioids (8 days of use per month), triptans (10 days of use per month), and NSAIDs (10-15
days per month

Neuropathy with Drugs

This patient has the classic presentation of acute polyneuropathy following oxaliplatin treatment.
Patients with acute oxalplatin polyneuropathy have increased sensitivity to touching cold items and
swallowing cold items (71%), throat discomfort (63%), and muscle cramps (42%). These symptoms peak
3 days after treatment. Electromyography in patients with acute oxaliplatin neuropathy demonstrates
spontaneous high frequency bursts of muscle unit action potentials and repetitive compound muscle
action potentials. Paclitaxol causes a chronic large and small-fiber sensory predominant polyneuropathy.
Thalidomide causes a distal sensory predominant polyneuropathy with tingling when tapping the
fingertips and autonomic neuropathy manifesting as constipation in more than 80% of patients.
Vincristine causes a distal sensory motor axonal polyneuropathy with more than a third of patients
having autonomic neuropathy, manifesting as orthostatic hypotension, constipation, bladder
dysfunction or impotence. polyneuropathy Following treatment with brentuximab vedotin, 50% of
patients treated with brentuximab had a sensory predominant polyneuropathy and 8% had a motor
predominant polyneuropathy.

Paroxysmal Kinegenic dyskinesia

Paroxysmal kinesigenic dyskinesia may be sporadic or inherited in an autosomal dominant fashion. It

responds well to low-dose anticonvulsants, such as carbamazepine.

Horner syndrome and response to drugs

This woman has right Horner syndrome, likely due to right internal carotid artery (ICA) dissection as a
result of chiropractic maneuvers. ICA dissection causes of oculosympathtic fibers that travel along the
extracranial ICA. With Horner syndrome of any cause (central, pre-ganglionic, post-ganglionic), there is
denervation hypersensitivity at post-ganglionic sympathetic receptors of the pupillary dilator muscle.
Apraclonidine is a weak alpha adrenergic agonist that binds to post-ganglionic receptors to cause
pupillary dilatation in all types of Horner syndrome. Hydroxyamphetamine will cause pupillary dilatation
in Horner syndrome of central (e.g. brainstem) and pre-ganglionic origin (e.g. Pancoast tumor), when
the third-order post-ganglionic neuron is intact (and can thus release norepinephrine in response to
hydroxyamphetamine). In carotid dissection, the post-ganglionic neuron is impaired and there is no
response to topical amphetamine. Topical cocaine produces no pupillary response in Horner syndrome,
82 as there is a synaptic deficit of norepinephrine. Pilocarpine in a cholinergic agent, producing pupillary
constriction and timolol is a beta-blocker, preventing pupillary dilatation.

Dacralizumab

Daclizumab is a humanized antibody that binds to CD25, the alpha subunit of the high-affinity
interleukin-2 (IL2) receptor expressed on T-lymphocytes. Through this interaction, daclizumab reduces
IL-2 signaling, which is thought to be important in the pathogenesis of MS and other autoimmune
disorders. In a randomized, double-blind study, daclizumab demonstrated significant reduction in
relapse rate (45%) and MRI activity when compared with intramuscular interferon beta-1a. Patients
treated with daclizumab had higher incidence of infection, cutaneous disorders, and transaminitis.
Autoimmune dermatitis and hepatitis have also been associated with daclizumab, and monthly
monitoring of liver enzymes has been mandated by the FDA for patients treated with daclizumab. ITP,
Goodpasture disease, and autoimmune thyroid disease have been associated with alemtuzumab, a CD-
52 monoclonal antibody, in patients with RRMS.