Prognosis for PBP patients is poor. Progressive bulbar palsy symptoms can include progressive difficulty with chewing, talking, and swallowing. Patients can also exhibit reduced gag reflexes, weak palatal movements, fasciculations, and weak movement of the facial muscles and tongue. In advanced cases of PBP, the patient may be unable to protrude their tongue or manipulate food in their mouth.

Patients with early cases of PBP have difficulty with pronunciations, particularly lateral consonants (linguals) and velars, and may show problems with drooling saliva. If the corticobulbar tract is affected a pseudobulbar affect with emotional changes may occur. Because PBP patients have such difficulty swallowing, food and saliva can be inhaled into the lungs. This can cause gagging and choking, and it increases the risk of pneumonia. Death, which is often from pneumonia, usually occurs 1 to 3 years after the start of the disorder.

Symptoms depend on the type of HSP inherited. The main feature of the disease is progressive spasticity in the lower limbs due to pyramidal tract dysfunction. This also results in brisk reflexes, extensor plantar reflexes, muscle weakness, and variable bladder disturbances. Furthermore, among the core symptoms of HSP are also included abnormal gait and difficulty in walking, decreased vibratory sense at the ankles, and paresthesia.

Initial symptoms are typically difficulty with balance, stubbing the toe or stumbling. Symptoms of HSP may begin at any age, from infancy to older than 60 years. If symptoms begin during the teenage years or later, then spastic gait disturbance usually progresses over many years. Canes, walkers, and wheelchairs may eventually be required, although some people never require assistance devices.

More specifically, patients with the autosomal dominant pure form of HSP reveal normal facial and extraocular movement. Although jaw jerk may be brisk in older subjects, there is no speech disturbance or difficulty of swallowing. Upper extremity muscle tone and strength are normal. In the lower extremities, muscle tone is increased at the hamstrings, quadriceps and ankles. Weakness is most notable at the iliopsoas, tibialis anterior, and to a lesser extent, hamstring muscles.

In the complex form of the disorder, additional symptoms are present. These include: peripheral neuropathy, amyotrophy, ataxia, mental retardation, ichthyosis, epilepsy, optic neuropathy, dementia, deafness, or problems with speech, swallowing or breathing.

Anita Harding classified the HSP in a pure and complicated form. Pure HSP presents with spasticity in the lower limbs, associated with neurogenic bladder disturbance as well as lack of vibration sensitivity (pallhypesthesia). On the other hand, HSP is classified as complex when lower limb spasticity is combined with any additional neurological symptom.

This classification is subjective and patients with complex HSPs are sometimes diagnosed as having cerebellar ataxia with spasticity, mental retardation (with spasticity), or leukodystrophy. Some of the genes listed below have been described in other diseases than HSP before. Therefore, some key genes overlap with other disease groups.

Progressive bulbar palsy (PBP) is a medical condition. It belongs to a group of disorders known as motor neuron diseases. PBP is a disease that attacks the nerves supplying the bulbar muscles. These disorders are characterized by the degeneration of motor neurons in the cerebral cortex, spinal cord, brain stem, and pyramidal tracts. This specifically involves the glossopharyngeal nerve (IX), vagus nerve (X), and hypoglossal nerve (XII).

This disorder should not be confused with pseudobulbar palsy or progressive spinal muscular atrophy. The term Infantile progressive bulbar palsy is used to describe progressive bulbar palsy in children. Some neurologists consider this disorder to be a subset of amyotrophic lateral sclerosis (ALS), but others disagree with that classification.

The extensor Babinski reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms – only muscles innervated by the damaged nerves will be symptomatic.

In the past, HSP has been classified as early onset beginning in early childhood or later onset in adulthood. The age of onsets has two points of maximum at age 2 and around age 40. New findings propose that an earlier onset leads to a longer disease duration without loss of ambulation or the need for the use of a wheelchair. This was also described earlier, that later onset forms evolve more rapidly.

In contrast to amyotrophic lateral sclerosis or primary lateral sclerosis, PMA is distinguished by the "absence" of:

- brisk reflexes

- spasticity

- Babinski's sign

- Emotional lability

As a result of lower motor neurone degeneration, the symptoms of PMA include:

- atrophy

- fasciculations

- muscle weakness

Some patients have symptoms restricted only to the arms or legs (or in some cases just one of either). These cases are referred to as "Flail Arm" (FA) or "Flail Leg" (FL) and are associated with a better prognosis.

People with the spastic/spasticity type of CP are hypertonic—i.e., they present with very stiff and tight muscle groups, far greater than typical humans—and have what is essentially a neuromuscular mobility impairment (rather than hypotonia or paralysis) which stems from an upper motor neuron lesion in the brain. The corticospinal tract or the motor cortex may be secondarily affected.

Spastic muscles are continuously contracting, or "tight", because the corresponding nerves permanently over-fire the command to tighten. This is caused by their inability to properly absorb GABA, or gamma amino butyric acid. The tightness, in addition to restricting movement, also acts as an overwhelming opposing force to neighbouring muscles and joints, eventually leaving the entire skeleton deformed compared to normal skeletal, bone, and joint structure in people without spasticity. Abnormal postures are usually associated with the antigravity muscles, which are extensors in the leg and the flexors in the arm. Deformities of joints develop which may become joint contractures, or "fixed contractures", with time.

Changes in spasticity and corresponding postures may also occur with other brain activity, such as excitement, fear or anxiety, or even pain, which increase muscle tension.

A person with spastic CP will commonly show, in addition to higher muscle tone, persistent primitive reflexes, greater stretch reflexes, plantar reflex, and ankle clonus.

A third of people with cerebral palsy have seizures - this is most common in spastic CP.

A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the ventral horn or anterior grey column of the spinal cord to the relevant muscle(s) – the lower motor neuron.

One major characteristic used to identify a lower motor neuron lesion is flaccid paralysis – paralysis accompanied by loss of muscle tone. This is in contrast to an upper motor neuron lesion, which often presents with spastic paralysis – paralysis accompanied by severe hypertonia.

Individuals with spastic diplegia are very tight and stiff and must work very hard to successfully resist and "push through" the extra tightness they perpetually experience. Other than this, however, these individuals are almost always normal in every significant clinical sense. When they are younger, spastic diplegic individuals typically undergo gait analysis so that their clinicians can determine the best assistive devices for them, if any are necessary, such as a walker or crutches. The main difference between spastic diplegia and a normal gait pattern is its signature "scissor gait"—a style that some able-bodied people might tend to confuse with the effects of drunkenness, multiple sclerosis, or another nerve disease. The degree of spasticity in spastic diplegia (and, for that matter, other types of spastic CP) varies widely from person to person. No two people with spastic diplegia are exactly alike. Balance problems and/or stiffness in gait can range from barely noticeable all the way to misalignments so pronounced that the person needs crutches (typically forearm crutches/lofstrand crutches) or a cane / walking stick to assist in ambulation. Less often, spasticity is severe enough to compel the person to use a wheelchair. In general, however, lower-extremity spasticity in spastic diplegia is rarely so great as to totally prevent ambulation—most people with the condition can walk, and can do so with at least a basic amount of overall stability. Regardless, it should be noted that from case to case, steeply varying degrees of imbalance, potential tripping over uneven terrain while walking, or needing to hold on to various surfaces or walls in certain circumstances to keep upright, are typically ever-present potential issues and are much more common occurrences amongst those with spastic diplegia than among those with a normal or near-normal gait pattern. Among some of the people with spastic diplegia who choose to be ambulatory on either an exclusive or predominant basis, one of the seemingly common lifestyle choices is for the person to ambulate within his or her home without an assistive device, and then to use the assistive device, if any, once outdoors. Others may use no assistive device in any "indoor" situation at all, while always using one when outdoors. Above the hips, persons with spastic diplegia typically retain normal or near-normal muscle tone and range of motion, though some lesser spasticity may also affect the upper body, such as the trunk and arms, depending on the severity of the condition in the individual (the spasticity condition affecting the whole body equally, rather than just the legs, is spastic quadriplegia, a slightly different classification). In addition, because leg tightness often leads to instability in ambulation, extra muscle tension usually develops in the shoulders, chest, and arms due to compensatory stabilisation movements, regardless of the fact that the upper body itself is not directly affected by the condition.

Spastic diplegia's particular type of brain damage inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma amino butyric acid (GABA), the amino acid that regulates muscle tone in humans. Without GABA absorption to those particular nerve rootlets (usually centred, in this case, around the sectors L1-S1 and L2-S2), affected nerves (here, the ones controlling the legs) perpetually fire the message for their corresponding muscles to permanently, rigidly contract, and the muscles become permanently hypertonic (spastic).

The abnormally high muscle tone that results creates lifelong difficulty with all voluntary and passive movement in the legs, and in general creates stress over time—depending on the severity of the condition in the individual, the constant spasticity ultimately produces pain, muscle/joint breakdown including tendinitis and arthritis, premature physical exhaustion (i.e., becoming physically exhausted even when you internally know that you have more energy than you are able to use), contractures, spasms, and progressively worse deformities/mis-alignments of bone structure around areas of the tightened musculature as the person's years progress. Severe arthritis, tendinitis, and similar breakdown can start as early as the spastic diplegic person's mid-20s (as a comparison, typical people with normal muscle tone are not at risk of arthritis, tendinitis, and similar breakdown until well into their 50s or 60s, if even then).

No type of CP is officially a progressive condition, and indeed spastic diplegia does not clinically "get worse" given the nerves, damaged permanently at birth, neither recover nor degrade. This aspect is clinically significant because other neuromuscular conditions with similar surface characteristics in their presentations, like most forms of multiple sclerosis, indeed do degrade the body over time and do involve actual progressive worsening of the condition, including the spasticity often seen in MS. However, spastic diplegia is indeed a chronic condition; the symptoms themselves cause compounded effects on the body that are typically just as stressful on the human body as a progressive condition is. Despite this reality and the fact that muscle tightness is the symptom of spastic diplegia and not the cause, symptoms rather than cause are typically seen as the primary area of focus for treatment, especially surgical treatment, except when a selective dorsal rhizotomy is brought into consideration, or when an oral baclofen regimen is attempted.

Unlike any other condition that may present with similar effects, spastic diplegia is entirely congenital in origin—that is, it is almost always acquired shortly before or during a baby's birth process. Things like exposure to toxins, traumatic brain injury, encephalitis, meningitis, drowning, or suffocation do not tend to lead to spastic diplegia in particular or even cerebral palsy generally. Overall, the most common cause of spastic diplegia is Periventricular leukomalacia, more commonly known as neonatal asphyxia or infant hypoxia—a sudden in-womb shortage of oxygen-delivery through the umbilical cord. This sudden lack of oxygen is also almost always combined with premature birth, a phenomenon that, even by itself, would inherently risk the infant developing some type of CP. On the other hand, the presence of certain maternal infections during pregnancy such as congenital rubella syndrome can also lead to spastic diplegia, since such infections can have similar end results to infant hypoxia.

The upper motor neuron lesion in the brain impairs the ability of some nerve receptors in the spine to properly receive gamma amino butyric acid (GABA). That leads to hypertonia in the muscles signaled by those damaged nerves. The limbs and body areas in which hypertonia manifests can be any or even all of them, depending which specific nerve groupings within the spine are rendered unable to receive GABA. Thus, spastic CP is often designated by body topography.

Facial paralysis is usually caused by traumatic, infectious, neurological, metabolic, toxic, vascular, and idiopathic conditions. While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease.

Usually beginning in one or both hands, MMN is characterized by weakness, muscle atrophy, cramping, and often profuse fasciculations (muscle twitching). The symptoms are progressive over long periods, often in a stepwise fashion, but unlike ALS are often treatable.

Sensory nerves are usually unaffected.

Wrist drop and foot drop (leading to trips and falls) are common symptoms. Other effects can include gradual loss of finger extension, leading to a clawlike appearance. Cold & hot temperatures exacerbates MMN symptoms to such an extent, unlike other neuropathies, that it is being investigated as a diagnostic tool.

Facial diplegia refers to people with paralysis of both sides of their face. Bilateral occurs when the onset of the second side occurs within one month of the onset of the first side. Facial diplegia occurs in 50% of patients with Guillain–Barré syndrome. Facioscapulohumeral muscular dystrophy (FSHD) is the second most common adult-onset muscular dystrophy with facial weakness being a distinct feature of FSHD in over 90% of cases.

Motor neuron diseases affect either upper motor neurons (UMN) or lower motor neurons (LMN), or both:

Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body.

The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only suffer minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.

Multifocal motor neuropathy (MMN) is a progressively worsening condition where muscles in the extremities gradually weaken. The disorder, a pure motor neuropathy syndrome, is sometimes mistaken for amyotrophic lateral sclerosis (ALS) because of the similarity in the clinical picture, especially if muscle fasciculations are present. MMN is thought to be autoimmune. It was first described in the mid-1980s.

Unlike ALS which affects both upper and lower motor nerves, MMN involves only lower motor nerves. Nevertheless, definitive diagnosis is often difficult, and many MMN patients labor for months or years under an ALS diagnosis before finally getting a determination of MMN.

MMN usually involves very little pain however muscle cramps, spasms and twitches can cause pain for some sufferers. MMN is not fatal, and does not diminish life expectation. Many patients, once undergoing treatment, only experience mild symptoms over prolonged periods, though the condition remains slowly progressive. MMN can however, lead to significant disability, with loss of function in hands affecting ability to work and perform everyday tasks, and "foot drop" leading to inability to stand and walk; some patients end up using aids like canes, splints and walkers.

Infants with spastic hemiplegia may develop a hand preference earlier than is typical.

A motor neuron disease (MND) is any of several neurological disorders that selectively affect motor neurons, the cells that control voluntary muscles of the body. They include amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), progressive bulbar palsy (PBP) and pseudobulbar palsy. Spinal muscular atrophies (SMA) are sometimes included in the group by some neurologists but it is different disease with clear genetic cause. They are neurodegenerative in nature and cause increasing disability and eventually, death.

Symptoms of HNA may include pain in the back, neck, arms, or shoulders, nerve pulls in the arms or back, muscular atrophy, and weakness.

Symptoms include intrinsic minus hand deformity, paralysis of intrinsic hand muscles, and C8/T1 Dermatome distribution numbness. Involvement of T1 may result in Horner's syndrome, with ptosis, and miosis. Weakness or lack of ability to use specific muscles of the shoulder or arm.It can be contrasted to Erb-Duchenne's palsy, which affects C5 and C6.

Clonus (i.e. involuntary, rhythmic, muscular contractions and relaxations) tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins. Some consider clonus as simply an extended outcome of spasticity. Although closely linked, clonus is not seen in all patients with spasticity. Clonus tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of clonus. Clonus results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups. Clonus is commonly seen in the ankle but may exist in other distal structures as well, such as the knee or spine.

Klumpke's paralysis (or Klumpke's palsy or Dejerine–Klumpke palsy) is a variety of partial of the lower roots of the brachial plexus. The brachial plexus is a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb. (see picture - click to enlarge). It is named after Augusta Déjerine-Klumpke.

Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements (such as chewing and speaking) and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech (which is often the initial presentation of the disorder), sometimes also demonstrating uncontrolled emotional outbursts.

The condition is usually caused by the damage (bilateral degeneration) to the neurons of the brain stem, specifically to the corticobulbar tract (upper motor neuron tract to cranial nerve motor nuclei).