After regular use, rebound insomnia may occur when discontinuing clonazepam. Benzodiazepines may cause or worsen depression. Occasional
Dysphoria
Induction of seizures or increased frequency of seizures
Personality changes
Behavioural disturbances
Ataxia

Rare
Suicide through disinhibition
Psychosis
Incontinence
Liver damage
Paradoxical behavioural disinhibition (most frequently in children, the elderly, and in persons with developmental disabilities)
Rage
Excitement
ImpulsivityThe long-term effects of clonazepam can include depression, disinhibition, and sexual dysfunction. Drowsiness
Clonazepam, like other benzodiazepines, may impair a persons ability to drive or operate machinery. The central nervous system depressing effects of the drug can be intensified by alcohol consumption, and therefore alcohol should be avoided while taking this medication. Benzodiazepines have been shown to cause dependence. Patients dependent on clonazepam should be slowly titrated off under the supervision of a qualified healthcare professional to reduce the intensity of withdrawal or rebound symptoms. Withdrawal-related
Anxiety
Irritability
Insomnia
Tremors
Headaches
Stomach pain
Hallucinations
Suicidal thoughts or urges
Depression
Fatigue
Dizziness
Sweating
Confusion
Potential to exacerbate existing panic disorder upon discontinuation
Seizures similar to delirium tremens (with long-term use of excessive doses)Benzodiazepines such as clonazepam can be very effective in controlling status epilepticus, but, when used for longer periods of time, some potentially serious side-effects may develop, such as interference with cognitive functions and behavior. Many individuals treated on a long-term basis develop a dependence. Physiological dependence was demonstrated by flumazenil-precipitated withdrawal. Use of alcohol or other CNS depressants while taking clonazepam greatly intensifies the effects (and side effects) of the drug. A recurrence of symptoms of the underlying disease should be separated from withdrawal symptoms. Tolerance and withdrawal
Like all benzodiazepines, clonazepam is a GABA-positive allosteric modulator.
Clonazepam has no effect on GABA levels and has no effect on gamma-aminobutyric acid transaminase. Clonazepam does, however, affect glutamate decarboxylase activity. It differs from other anticonvulsant drugs it was compared to in a study.Clonazepams primary mechanism of action is the modulation of GABA function in the brain, by the benzodiazepine receptor, located on GABAA receptors, which, in turn, leads to enhanced GABAergic inhibition of neuronal firing. Benzodiazepines do not replace GABA, but instead enhance the effect of GABA at the GABAA receptor by increasing the opening frequency of chloride ion channels, which leads to an increase in GABAs inhibitory effects and resultant central nervous system depression. In addition, clonazepam decreases the utilization of 5-HT (serotonin) by neurons and has been shown to bind tightly to central-type benzodiazepine receptors. Because clonazepam is effective in low milligram doses (0.5 mg clonazepam = 10 mg diazepam), it is said to be among the class of "highly potent" benzodiazepines. The anticonvulsant properties of benzodiazepines are due to the enhancement of synaptic GABA responses, and the inhibition of sustained, high-frequency repetitive firing.Benzodiazepines, including clonazepam, bind to mouse glial cell membranes with high affinity. Clonazepam decreases release of acetylcholine in the feline brain and decreases prolactin release in rats. Benzodiazepines inhibit cold-induced thyroid-stimulating hormone (also known as TSH or thyrotropin) release. Benzodiazepines act via micromolar benzodiazepine binding sites as Ca2+ channel blockers and significantly inhibit depolarization-sensitive calcium uptake in experimentation on rat brain cell components.