and E. Lee Murray, MD
CHAPTER CONTENTS
SPASTICITY
Spasticity is common with a wide range of neurologic diseases. Management can be difficult and is almost always multimodal, although not all patients need treatment other than maintaining activity. However, management is considered especially when the patient has intractable pain or significant limitation of motion because of the spasticity.
Physical therapy should be considered first-line for almost all patients. The type and extent of therapy depend on the severity of the deficit.
Baclofen is a gamma aminobutyric acid (GABA) agonist commonly used for spasticity. Initial treatment is usually orally, but it is very effective intrathecally, given by continuous pump. Overdose can produce severe encephalopathy. A common starting dose is 5 mg t.i.d.
Benzodiazepines are commonly used, especially diazepam and clonazepam. They often cause sedation; this is most prominent initially and on dose increments.
Dantrolene is an alternative especially to baclofen. Because of the mainly peripheral action, it is less likely to produce cognitive effects at therapeutic doses. Starting dose is usually 25 mg/day.
Tizanidine is a newer agent that may produce less reduction in muscle function than the other agents described. Starting dose is often 2 mg q6-8h prn, max 3 doses/day.
Botulinum toxin injections is used for spasticity and focal spasms. Because of the size of the muscle mass involved, patients with widespread spasticity may not be a candidate for this treatment.
Surgery of various sorts can be done for spasticity. Some of these approaches can include contracture release, osteotomy, and implantation of a pump. Selective dorsal rhizotomy is considered for medically refractory cases.
INCREASED INTRACRANIAL PRESSURE
Intracranial pressure (ICP) can be increased from a wide variety of conditions discussed in this book. Generally, the causes fall into the following categories:
•Obstruction of CSF absorption
PRESENTATION depends on etiology and acuteness. Common symptoms include headache, nausea, vomiting, visual change including blurring or diplopia, and, ultimately, confusion, lethargy, and pupillary dilation. Diplopia from increased ICP is usually horizontal and due to abducens palsy. Visual change can be blurring to blindness. Papilledema is seen on exam unless the ICP increase is very acute. Additional brainstem findings can be from displacement and compression of neural structures as well as ICP itself.
DIAGNOSIS is discussed in depth throughout this book. Imaging is performed urgently when increased ICP is suspected.
MANAGEMENT is individualized on the basis of cause, acuity, and severity, but some general tools include:1
