MORE ON SCHIAVO & MALKIN

You can find a PDF version of the autopsy report here and I previously posted some excerpts that I typed in from this PDF. Thanx to the miracle of PDF -> Word conversion, I now have a Word 97-2003 version and I can e-mail it to you if you'd like. Just leave your address in the comment section. Tbogg also has some thoughts on Malkin's psychopathology.

Here are some excerpts from the neuropathologist (Steven J. Nelson) that are relevant to the "debate":

At autopsy, the brain weighed 615 grams. A total of 645 milliliters of cerebrospinal fluid (weighing 678 grams) were recovered upon opening the skull and exposing the brain. The brain was small, with widened sulci and narrow and thinned gyri. It was smaller in its vertical dimension as a result of the hydrocephalus ex vacuo tissue volume loss. The worst affected areas were the bilateral occipital lobes.

The deep midline nuclei of the cerebellum were symmetric and the folia demonstrated significant golden-brown discoloration and widespread atrophy.

The changes seen were striking in their appearance, and global in their distribution. They predominately involved the border zone ("watershed") areas and were most severe in the occipital lobes, with relative preservation of the frontal and temporal lobes. There was a readily discernible and noteworthy gradient loss when moving from the anterior to posterior regions. In the thalamus, the most medial portions were relatively preserved (from the frontal cortex). In the basal ganglia, the corpus striatum all but vanished, replaced by extensive astrocytosis (caudate nucleus greater than putamen). This volume loss was impressive and was all but completely represented by non-neoplastic astrocytes. An occasional rare neuron was located. The frontal and temporal poles and insular cortex demonstrated relative preservation. The granular neurons of the cerebral cortex were relatively preserved, while the larger pyramidal neurons were globally absent. There was laminar necrosis involving the middle cortical lamina, in most cortical sections examined microscopically, but this finding was patchy. Hyaline sclerosis of many of the smaller microscopic arterioles was noted and many arterioles also contained widely dilated perivascular spaces. There were calcific vasopathic changes and diffuse astrocytosis in the globus pallidus.

The pyramids demonstrated pyramidal tract Wallerian degeneration. Damage to the midbrain, including the red nuclei, appeared related to Wallerian degeneration from fibers passing through these neuroanatomic structures. The lateral geniculate nucleus (visual) demonstrated transneuronal degeneration with gliosis, while the medial geniculate nudeus (auditory) was relatively preserved. The hippocampal formations demonstrated diffuse neuronal loss (CA 1 thru CA4, and endplate) associated with reactive astrocytosis.

Within the cerebellum there were no recognizable Purkinje cells found. The lost Purkinje neurons were replaced by reactive Bergmann astroglia. In the pons the descending fiber pathways were most affected. The inferior olivary nuclei had no remaining discernable neurons, suggesting this was a retrograde degeneration due to the marked cerebellar cortex damage. The deep midline cerebellar nuclei were relatively preserved, but with prominent astrocytosis.

Comment: Brain weight is an important index of its pathologic state. Brain weight is correlated with height, weight, age, and sex. The decedent's brain was grossly abnormal and weighed only 615 grams (1.35 lbs.). That weight is less than half of the expected tabular weight for a decedent of her adult age of 41 years 3 months 28 days. By way of comparison, the brain of Karen Ann Quinlan weighed 835 grams at the time of her death, after 10 years in a similar perisistent vegetative state'.

Neuropathologic examination alone of the decedent's brain — or any brain, for that matter —cannot prove or disprove a diagnosis of persistent vegetative state or minimally conscious state.

Here are some excerpts from the medical examiner (Jon R. Thogmartin)

3. Could Mrs. Schiavo eat by mouth?

The neuropathologic findings, oropharyngeal anatomic findings, and medical records clearly indicate that Mrs. Schiavo would not have been able to consume sustenance safely and/or in sufficient quantity by mouth. In fact, the records and findings are such that oral feedings in quantities sufficient to sustain life would have certainly resulted in aspiration. Swallowing evaluations and speech pathology evaluations repeatedly record that Mrs. Schiavo was a high risk for aspiration and not a candidate for oral nutrition/hydration. Although in her early rehabilitation, she received speech pathology services, she was later repeatedly evaluated and determined not to be a candidate for speech/dysphagia therapy. According to medical records, she had been treated in the past for aspiration pneumonia. Thus, Mrs. Schiavo was dependent on nutrition and hydration via her feeding tube. Claims from caregivers of past oral feedings are remarkable, and, based on the autopsy findings and medical records, these feedings were potentially harmful or, at least, extremely dangerous to Mrs. Schiavo's health and welfare.

5. What diagnoses can be made in regards to the brain of Mrs. Schiavo? (See attached neuropathology report)

Mrs. Schiavo's brain showed marked global anoxic-ischemic encephalopathy resulting in massive cerebral atrophy. Her brain weight was approximately half of the expected weight. Of particular importance was the hypoxic damage and neuronal loss in her occipital lobes, which indicates cortical blindness. Her remaining brain regions also show severe hypoxic injury and neuronal atrophy/loss. No areas of recent or remote traumatic injury were found.