Clinical Pathophysiology Volume 2 – Phillip Tisdal

There are many causes, but the commonest causes can be classified into: ▪ Childhood: • Congenital: o Stenosis of the aqueduct (idiopathic): most common cause o Malformations (see Chapter 12. Embryology, developmental and congenital disorders). ▪ Dandy-Walker malformation: obstruction of foramina of Magendie and Luschka leading to cerebellar atrophy ▪ Chiari malformations: protrusion of cerebellum into the spinal canal, with obstruction of foramina • Acquired: o Neoplasia (and infection and hemorrhage): most childhood CNS neoplasms are infratentorial.

Increased ICP causes headache and cerebellar involvement causes ataxia. ▪ Adults • Normal pressure hydrocephalus (NPH) o Most childhood hydrocephalus is due to obstruction in ventricular drainage (aka non-communicating hydrocephalus). ▪ Presentation: depends upon whether or not there is fusion of the cranial sutures. • Before closure, the children develop large heads with few early symptoms.

o P/E shows increased head circumference • After closure, there is rapid increase in ICP with destruction of brain tissue. o Symptoms usually include headache along with neurologic abnormalities o Signs include dorsal mid-brain pathology ▪ Sunset eyes: at rest, there is downward gaze and sclera above the irises. (See Chapter 12. Figure 12-12). ▪ Parinaud syndrome (dorsal midbrain): vertical gaze palsy, pupillary near-light dissociation, lid retraction, convergence-retraction nystagmus • Diagnosis: imaging to show ventricular dilation, ↑CSF pressure, usually measured by a surgically implanted ventricular pressure transducer.

▪ Adults: normal pressure hydrocephalus (NPH) • An idiopathic disease with ventricular dilation. This is associated with the triad of: gait disturbance (most important), incontinence and dementia. Spinal tap has a normal opening pressure. • This is presumed to be a disease of decreased absorption of CSF by the arachnoid granulations. >50% of NPH patients have granulation fibrosis. The commonest cause is hemorrhage. ▪ This is one of the few reversible causes of dementia (also reversible are: depression, alcoholism and subdural hematoma).

Triad of NPH: • Wet (incontinence) • Wacky (dementia) • Wobbly (ataxia) Abnormal gaits • Antalgic: to avoid pain (e.g. osteoarthritis) • Ataxia: uncoordinated (cerebellar, sensory & vestibular) • Magnetic: as feet are adherent to the ground (e.g. NPH) Pathophysiology Idiopathic Intracranial Hypertension (IIH, aka Pseudotumor cerebri) An idiopathic disease of obese women of childbearing age.

Presentation: only signs of ↑ICP o Symptoms: headache o Signs: papilledema o Testing: ▪ MRI: normal ▪ CSF: increased opening pressure, normal fluid Pathophysiology: unknown Natural history: o Complications: loss of vision due to papilledema o Treatment: loss of weight, acetazolamide Premature infants and periventricular leukomalacia and hemorrhage (GMH-IVH) o Development of the cerebral cortex seems to require ventricles.

The CSF formed in choroid plexus of the ventricles carries the growth factors and other signals necessary for embryologic development.

When this author started medical school in 1972, the knowledge that DNA was double-stranded was only 20 years old. Anatomy was taught using cadavers because these were the best models available. The first CT scanner would not be used in North America until 1973. By 1980, there would be 3 million. With the parallel development of MRI and ultrasound, every doctor would soon use these tools to see the internal anatomy of their patients. Imaging would radically decrease the importance of the less sensitive and specific physical examination.

In the 1970’s laboratory testing saw the first of its automated instruments in chemistry and hematology. Now, an estimated 60-70% of medical decisions are based on laboratory testing. There is non-invasive testing for glucose, bilirubin, O2 , CO2 and pH. We are just entering the “omics” era of proteomics, pharmacogenomics, nutrigenomics, and physiogenomics that will individualize patient care.

All of these developments blend clinical care and basic sciences. Despite the fact that clinical medicine can now be built on a foundation of the basic sciences, medicine is still taught by subjects. These are learned far from the bedside and are mostly forgotten by the clerkship years of medical school. This book is an attempt to teach medicine from a patient-centered approach. There is a list of the more than four dozen of the most important chief complaints and their differential diagnosis, indexed to the text.

Every organ system starts with a clinical pathologic correlation that shows that organ’s commonest presentations and the associated diseases. There is a review of each organ’s essential structure and function in its clinical context. Diseases are described through their presentation, pathophysiology, and natural history. There are no individual subjects, just the information needed to understand and care for the patient. When I was a clinical clerk, an outstanding doctor told me that all I needed to learn medicine was my patients and my books.

That is still good advice. This book is intended to help any physician teach themselves medicine by better understanding what they should be learning from their patient care. Philip Tisdall Preface Clinical Pathophysiology (Volume 2) ©2024 Copyright by Philip Tisdall M.D. All rights reserved. This book is protected by copyright.

This is a short excerpt from the opening of “” by Unknown, quoted for review and introduction purposes. All rights belong to the copyright holders.

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