The pathophysiology of spasticity is a complex subject and one frequently avoided by clinicians. Spasticity and the other features, positive and negative, of the upper motor neurone (UMN) syndrome arise from disruption of certain descending pathways involved in motor control. Hyperexcitability of spinal reflexes forms the basis of most of the positive clinical signs of the UMN syndrome, which have in common excessive muscle activity. These spinal reflexes may be divided into two groups, proprioceptive reflexes and nociceptive/cutaneous reflexes. The clasp-knife phenomenon combines features of both groups, at least in the lower limbs. Contractures are a well known and feared complication of the UMN syndrome, reducing the range of motion of a joint. There has been a recent investigation of the relationship between the stretch reflex hyper excitability of spasticity and contractures. Spasticity does not appear to exist in contracting agonists and would not really interfere with movement.

A detailed neurological history allows one to focus on important components of the neurological examination and for saving time and resources. The important elements of a focused neurological examination include onset of symptoms, temporal relationships of symptoms, progression of symptoms, associated symptoms, exacerbating and alleviating factors, symptoms that indicate involvement of a particular region of central nervous system (CNS), history of similar event and history of medication use. This chapter describes the examination of mental status, cranial nerve function, motor function, deep tendon reflexes, cutaneous reflexes, and miscellaneous signs, sensory modalities, and pathological reflexes. The Glasgow Coma Scale is often used as a method of briefly quantitating neurological dysfunction. A simple method to remember the anatomic basis of neurological examination is to focus on five levels of the CNS, which are the brain, the brainstem, the spinal cord, the peripheral nerves, and the muscles.