Ethicon's Case Study

Published on: August 19, 2024


On June 17, 2002, the superior court sustained Ethicon's demurrer to the products liability cause of action without leave to amend, relying upon Norgart, supra, 21 Cal.4th 383, 87 Cal.Rptr.2d 453, 981 P.2d 79, and Bristol-Myers Squibb, supra, 32 Cal.App.4th 959, 38 Cal.Rptr.2d 298, to conclude that the statute of limitations barred the products liability cause of action. The superior court stated that when a plaintiff sues based on knowledge or suspicion of negligence, including medical malpractice as in Fox's case, the statute of limitations begins to run as to all defendants, including manufacturers possibly liable under products liability theories. The superior court also stated that Fox failed to demonstrate that amending the complaint could ""overcome the limitations defense."" Fox timely appealed from the superior court's order sustaining Ethicon's demurrer as to the products liability cause of action.

The Court of Appeal reversed the superior court's order and remanded with directions to grant Fox leave to amend to allege facts explaining why she did not have reason to discover earlier the factual basis of her products liability claim. In so ruling, the Court of Appeal held that Bristol-Myers Squibb's ""bright-line rule of imputed simultaneous discovery of causes of action"" did not apply. Ethicon petitioned this court, and we granted review.

additional questions

 Question 1

A 25-year-old woman, pregnant in her second trimester, starts to

experience chorea and bilateral ankle arthralgia but has no past history of

rheumatic chorea. In the first hour, her erythrocyte sedimentation rate is

70. Could this be no more than chorea gravidarum?

Question 2

Is valproate as equally effective as haloperidol in the treatment of chorea,

in particular rheumatic chorea?

Question 3

Does a lesion of Guillain-Mollaret's triangle in the brain stem cause a

type of myoclonus other than symptomatic palatal myoclonus?

Question 4

1. In West's syndrome, after the fits have been suppressed, for how

long should treatment with adrenocorticotrophic hormone (ACTH)

continue?

2. Does complete suppression of resistant infantile myoclonic jerks by

ACTH characterize West's syndrome?

Question 5

Are anticholinergics the first line of treatment for primary torsion

dystonia?

Question 6

Can multiple sclerosis (MS) be associated with lack of vitamin D,

lack of sunlight or low fish/cod-liver oil in the diet? By looking at the

epidemiology (none at the equator; more outside 40 latitude, both north

and south; less on top of Swiss mountains than in the Swiss valleys; more

in fishing coastal towns and in Eskimos) this seems to be very important.

Vitamin D modulates the immune system and active vitamin D given

to rats with experimental MS (acute encephalomyelitis) lowers the

monocyte count in cerebrospinal fluid (CSF) by 90% in 72 hours with

return of power to their limbs. Japanese MS patients who ate plenty of

fish were found to have vitamin-D-receptor pleomorphism. The staple

grains and cereals (wheat, barley, oats) eaten in Scandinavian and

northern European countries contain phytic acid, which blocks vitamin D

absorption, and rice is the only cereal free of phytic acid.

Are there any studies where low vitamin D levels in blood are

associated with MS relapse?

Question 7

What are the diagnostic criteria of 'definitive' multiple sclerosis (MS) - as

taught to a medical student? We have found different information from

different sources.

Question 8

How reliable is a CT-brain scan with contrast in showing MS lesions as

enhancing lesions in the presence of a contraindication to use MRI?

Question 9

Is magnetic resonance (MR) spectroscopy of value in differentiating

multiple sclerosis from cerebral autosomal dominant arteriopathy with

subcortical infarctions (CADASIL)?

Question 10

Does hemiplegia due to multiple sclerosis present with hemiparesis

rather than dense hemiplegia (which is more characteristic of a stroke)?

Other than age, what are the clinical signs that would help differentiate

between the two?130"

Can a 25-year-old pregnant woman with chorea and bilateral ankle arthralgia, ESR 35mm/hr be having chorea gravidarum?

 

 It may well be that the woman is suffering from chorea gravidarum and this is a condition that occurs during pregnancy. This is so because the elevated erythrocyte sedimentation rate indicates inflammation which is a characteristic of this diseases.

 As effective as haloperidol in the treatment of chorea, especially rheumatic chorea, is valproate?

 

 Haloperidol is usually preferred over valproate in the management of rheumatic chorea since it forms part of the standard treatment for chorea-associated conditions.

 Does a lesion of Guillain-Mollaret’s triangle in the brainstem cause any other type of myoclonus than symptomatic palatal myoclonus?

 

 Indeed, a lesion of Guillain-Mollaret’s triangle can cause different types of myoclonus, including generalized myoclonus, not only symptomatic palatal myoclonus.

 In West’s syndrome, following the control of fits, for how long should the child be treated with adrenocorticotrophic hormone (ACTH)? Is complete suppression of resistant infantile myoclonic jerks by ACTH diagnostic of West’s syndrome?

 

 ACTH therapy for West’s syndrome is usually given for at least three months, and may be given for as long as four to six weeks. Absence of resistant infantile myoclonic jerks on ACTH does not always point to West’s syndrome but shows treatment effect.

 Are anticholinergics the first choice of treatment for primary torsion dystonia?

 

 Anticholinergics are not used as a first line of treatment for primary torsion dystonia. Dopamine agonists and deep brain stimulation are the first-line treatments, but for severe cases.

 Is there evidence that link Multiple Sclerosis (MS) with low Vitamin D levels and are there any studies that show that low levels of Vitamin D increases the chance of relapse of MS?

 

 Indeed, low vitamin D levels have been linked to multiple sclerosis. A cohort study also established that patients with MS have low levels of vitamin D and also that low levels of vitamin D are associated with increased relapse rates, pointing towards a possible role in disease activity.

 What are the diagnostic criteria that are used for the diagnosis of MS in its ‘definitive’ form?

 

 The diagnostic criteria for 'definitive' MS include:The diagnostic criteria for 'definitive' MS include:

 Temporal and geographical spread: presence of multiple events and multiple lesions in different regions of the body.

 The signs and symptoms are in conformity with the diagnosis of MS.

 Exclusion of other diagnoses.

 Typical MRI changes of MS were present.

 Tyndallisation and csf analysis showing oligoclonal bands.

 To what extent can the CT-brain scan with contrast be used to display MS lesions as enhancing lesions in the presence of a contraindication to MRI?

 

 CT scans with contrast are less sensitive than MRI scans in the detection of the MS lesions especially the enhancing lesions. MRI is more useful in the diagnosis of MS but if contrast MRI is contra indicated then CT can be of some value.

 Is magnetic resonance (MR) spectroscopy helpful in the differential diagnosis of multiple sclerosis from cerebral autosomal dominant arteriopathy with subcortical infarctions (CADASIL)?

 

 MRS can also be of value in distinguishing between MS and CADASIL, since it allows for consideration of the metabolic alterations in the head. MS usually has low NAA and high Cho signals; CADASIL may present with different MR spectroscopy findings.

 Can one have hemiplegia secondary to multiple sclerosis and not have the dense hemiplegia but rather hemiparesis? Which clinical features may be used to distinguish it from the stroke?

 

 Affection of the upper limb is less severe than the lower limb in hemiplegia due to multiple sclerosis, the patient may have hemiparesis rather than dense hemiplegia. Clinical signs to differentiate MS from stroke include:Clinical signs to differentiate MS from stroke include:

 Onset and progression: MS has a somewhat more gradual onset and the symptoms are not necessarily constant and may change.

 Pattern of symptoms: It is for this reason that MS symptoms may come and go while stroke symptoms are fixed and do not change.

 Associated symptoms: MS may be associated with other neurological finding such as sensory deficit or optic neuritis.


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